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Final Micr 386
| Term | Definition |
|---|---|
| cytokines | low molecular weight regulatory proteins or gylcoproteins secreted by leukocytes and various other cells in response to various stimuli |
| cytokines are generally ____ messengers of the immune system but can be ______ | local, systemic |
| lymphokine | secreted by lymphocytes |
| monokine | secreted by monokines |
| interleukin | large group of cytokines that promote cell to cell interactions and stimulate humoral or cell mediated immune responses |
| tumor necrosis factor | protein produced chiefly by monocytes and macrophages in response to endotoxins |
| tumor necrosis factor mediates ____, induces destruction of ____ ___ and activates ____ ____ ___ | inflammation, tumor cells, white blood cells |
| interferon | group of glycoproteins produced and secreted by certain cells |
| interferon induces _______ state in other cells and ____ immune system | antiviral, regulates |
| chemokines | group of secreted low molecular weight polypeptides that mediates chemotoxins for different leukocytes and regulates adhesion of leukocytes |
| cytokines exhibit ___ ___ affinity for receptors | very high |
| cytokines are mainly produced by ___, ____ and ____ | helper T cells, dendritic cells, macrophages |
| cytokines are messengers ____ innate and adaptive immune system | between |
| cytokines are produced by activated ____ and induce ____ ____ | macrophages, inflammatory response |
| IFN-alpha, IFN-beta and IFN-gamma create ___ ___ in cell | antiviral state |
| cytokines can act as cell ___ ___ ___ during immune responses | growth response factors |
| ____ to tissue elicits inflammation which triggers cytokines to begin ___ | damage, healing |
| cytokines regulate ____ and ___ of the immune response by influencing ____ and ____ of cells of the immune system | magnitude, nature, growth, differentiation |
| pleiotropy | single cytokine can produce multiple effects either by on single or multiple cell types |
| redundancy | multiple cytokines can target the same cells to elicit same effect |
| synergy | combined cytokine effect is greater than added effect of each separately |
| antagonism | cytokines can act to block the effects of other cytokines |
| IL-1B, IL-6 and TNF-alpha are all ____ cytokines | proinflammatory |
| IL-10 and TGF-beta are ___ cytokines | antiinflammatory |
| IL-2, IL-4 and IL-12 are important for ___ | T cells |
| IL-4, IL-5 and IL-7 are important for ___ | B cells |
| immunoglobuin super family receptors have the same immunoglobulin domain structure found in ____ and ____ | MHC, immunglobulin |
| __ is a proinflammatory cytokine that plays an important role in inducing fever through stimulation of the ____ | IL-1, hypothalamus |
| class I cytokine receptors have a ___ amino acid motif | Trp-Ser-X-Trp-Ser |
| IL-3, 5, 6, 12, 13 are all | class I cytokine receptors |
| Il-2 assist in proliferation of | CD4+ cells |
| pIL-4 promotes differentiation of activated T cells into ___ ___ _ cells | T helper 2 |
| IL-7 is required to drive proliferation and survival of ___ ___ cells into __ ___ __ cells | pre B, late pro B |
| class II cytokine receptors are similar in structure to class I but do not have same ___ ___ ___ | amino acid motif |
| class II cytokine receptors are characterized by ____ ___ | disulfide bonds |
| class I cytokine receptors are also known as | hematopoetin receptor family |
| class II cytokine receptors are also known as | interferon receptor family |
| characteristics of interferon | pleiotropy, redundancy, synergy, antagonism |
| TNF receptor family has ___ rich domains | cysteine |
| Chemokine receptors are ___ ___ ___, containing 7 transmembrane domains | G protein coupled |
| ___ and ___ are coreceptors for HIV | CCR5, CXCR4 |
| Th1 cells are a subset of helper T cells responsible for ______ immunity | cell mediated |
| Th2 cells are a subset of helper T cells responsible for ___ immunity | humoral |
| In Th1 induction ___ secrete IL-2 which promotes differentiation through activation of ___ | APC, STAT4 |
| In Th2 induction ____ and ___ secrete IL-4 which promotes differentiation through activation of ____ | basophils, mast cells, STAT6 |
| ___ is the main pathway associated with cytokine signalling as a result of T cell commitment | JAK-STAT |
| JAK | janus kinase |
| JAK is a family of intracellular ____ ___ ____ that transduce cytokine mediated signals in JAK-STAT pathway | nonreceptor tyrosine kinase |
| STAT | signal transudcers and activators of transcription |
| STAT is a family of intracellular transcription factors that mediate aspects of cellular ____ and ____ | proliferation, differentiation |
| step 1 of JAK-STAT signalling | cytokine binds to cytokine receptor causing it to dimerize |
| step 2 of JAK-STAT signalling | activation of JAK family tyrosine kinases resulting in phosphorylation of receptor |
| step 3 of JAK-STAT signalling | tyrosine phosphorykation of STAT by JAK |
| step 4 of JAK-STAT signalling | dimerization of STAT |
| step 5 of JAK-STAT signalling | translocation of STAT in to the nucleus binding to DNA |
| step 6 of JAK-STAT signalling | specific gene transcription commiting the T cell to Th1/2 lineage |
| secrete cytokines either | inhibit proliferation of other subset enhance proliferation of its own subset through positive feedback |
| sepsis | body's extreme response to infection that results in life threatening condition which causes tissue damage, organ failure and death |
| gram negative cell wall endotoxins cause overproduction of __ and ___ by macrophage | IL-1, TFN-alpha |
| shock state | characterized by hypotension, severe pulmonary edema and hemorrhage |
| bacterial septic shock amplifies ___ ___ of nearby cells and macrophages to secrete additional ____ ___ | inflammatory cascade, proinflammatory cytokines |
| bacterial toxic shock is a result of infectious bacteria releasing ____ and causes fever and swelling | superantigens |
| release of superantigens causes nonspecific activation of ___ ___ and creates a ___ ___ | T cells, cytokine storm |
| plasmacytosis | condition which there is an unusually large proportion of plasma cells in tissues, blood or excreted fluid |
| overproduction of __ leads to exaggereated cell proliferation | IL-6 |
| clonal expansion occurs as a result of ___ recombination | VDJ |
| clonal expansion results in proliferation of B cell clones if | the mature B cells encounter an antigen |
| ___ ___ response describes the first encounter with a given antigen | primary immune |
| primary immune results in activation and differentiation of ___ B cells into ___ B cells | naive, plasm |
| naive B cells | mature B cells that has not yet encountered an antigen |
| ___ is the first antibody produced | IgM |
| __ ___ cells remain in circulation after antibody concentration has diminished | memory B |
| __ describes the immune responses to a subsequent counter of a specific antigen | secondary |
| there is a much more rapid shift to production of ___ | IgG |
| ___ overall antibody concentration is sustained for a __ time period | higher, longer |
| titre | concentration of antiserum, last dilution of antiserum capable of mediating some measureable effect |
| hapten | small antigen not immunogenic unless attached to large carrier molecule |
| The measureable effects of titre include ____ or ___ of antigen | precipitation, agglunination |
| when a host has been previously exposed to hapten carrier conjugate, reexposure to same carrier leads to weaker immune response than unrelated carrier, true or false | False, it leads to a stronger immune response |
| the plasma cell survival niche is found in the ___ ___ | bone marrow |
| the plasma cell survival is thought to support dynamic needs of __ and __ | essential factors, memory B cells |
| essential factors include | IL-5, IL-6, TNF-alpha |
| multiple myeloma is cancer of plasma cells in the bone marrow, true or false | true |
| multiple myeloma is likely associated with deregulatio of __ __ __ or __ __ __ __ | bone marrow microenvironment, plasma cell survival niche |
| dutcher bodies are associated with ___ ___ in perinuclear cytoplasm with subsequent invagination in nucleus | immunogen accumulation |
| mott cells are ___ ___ inclusions full of russel bodies | spherical cytoplasm |
| russell bodies are eosinphilic immunoglobulin containing inclusions found in plasma cells undergoing __ __ __ | excessive Ig synthesis |
| Hoskins effect | antigenic shift or drift of viruses poses a major challenge |
| hoskins effect is also known as | original antigenic shift |
| primary immune response sees relatively ___ antibody production compared to secondary | low |
| during a secondary immune response, antibody levels will remain ___ for___ than during primary | high, longer |
| during first exposure there is a lag period of ___ days as naive B cells differentiate into plasma cells | 4-7 |
| during secondary, the lag period is shortened to __ days due to the presence of ___ B cells | 1-3, memory |
| In primary exposure, IgM is produced at nearly ___ levels as IgG | same |
| True or false: during a secondary immune response, IgG is produced at much lower levels than IgM to allow for greater antigen affinity | false, it is produced at much higher levels |
| three signals of B cell activation | TCR-MHC II complex binding, costimulatory molecule signaling, cytokine signaling |
| BCR (___) on naive B cell binds to its antigen (__) | Ig, Ag |
| Ig-Ag is internalized by ___ ___ ___ | receptor mediated endocytosis |
| antigen is processed via ____ pathway and displayed by MHC II on cell surface | endocytic |
| True or false, CR recognizes processed antigen:MHC complex presented by B cells leading to TCR and CD4 binding to complex | true |
| CD40L expression is induced on helper T ceels through ___ ___ __ | inositol lipid hydrolysis |
| inositol lipid hydrolysis | inositol lipids on cell membrane are hydrolyzed |
| PIP2 | inositol lipids |
| ___ on helper T cell interact with ___ on B cells | CD40L, CD40 |
| CD40L-CD40 binding activates ___ ___ expression on both B and T cells | cytokine |
| True or false: MHC II mediated cAMP activation results in decreased expression on B cells | False, it leads to increased expression on B cells |
| ___ binds to ___ on T cell, activating helper T cell | B7, CD28 |
| B7-CD28 interaction induces ___ cascade | MAPK |
| MAPK | mitogen activated protein kinases |
| MAPK cascade triggers __ and ___ to form AP-1 that induces activation of IL-2 gene | cJUN and cFos |
| after MAPK cascade, cytokines thenbind to respective recepotrs initiating | proliferation and differentiation |
| step 1 of cytokine secretion | TCR:MHC, CD40L:CD40, LFA-1:ICAM-1 interactions promotes talin mobilization to point of cell:cell contact |
| step 2 of cytokine secretion | helper T cell reorganizes cytoskeleton toward B cell so cytokines can be released close to point of contact between B and T cell |
| step 3 of cytokine secretion | T cell secretes IL-4 directly toward B cell point of contact |
| outcome of three signals of B cell activation | proliferation or differentiation |
| during B cell proliferation, cells enter __ cell cycle, occurs following additional ___ costimulating signal from activated macrophages as well as ___, ___, and ___ to promote clonal expansion | G1, IL-1, IL2, 4, 5 |
| during B cell differentiation cytokines released by helper T cells induce __ __ | class switching |
| IFN-gamma induces | IgG |
| IL-5 and TGF-beta induce | IgA |
| IL-4, 5 and 13 induce | IgE |
| IL-4, 2, 5 induce | IgM |
| hyper IgM syndrome is an | x linked trait |
| HIGM occurs when there is a defect/deficiency in | CD40L |
| HIGM results in T cells incapable of inducing ___ __ from IgM | class switching |
| Type 1 T cell independent antigens are also known as | polyclonal B cell activators |
| Type 1 T cell independent antigens are capable of activating B cells regardless of ___ ___ | antigen specificity |
| an example of Type 1 T cell independent antigens is | lippopolysaccharides |
| type 2 T cell independent antigens are expressed on __ of __ in organized and highly reptitive manner | surface, pathogens |
| Type 2 T cell independent antigens activate B cells by extensively ___ ___ membrane bound immunoglobulin in a multivalentfashion | crosslinking |
| an example of Type 2 T cell independent antigens is | bacterial cell wall polysaccharides |
| effector cells are cells that have a ____ ____ rather than regulatory effect | biological function |
| effector cells mediates ______ immunity | cell mediated |
| nonspecific responses are performed by __ and ___ | marcophages, natural killer cells |
| nonspecific responses result in increased __ and __ | IFN-alpha, IFN-beta |
| specific responses are performed by ___ | cytotoxic T cells |
| nonspecific cells | can recognize pathogens but are not specific to a particular antigen |
| specific cells | specific for a processed pathogen antigen complex with MHC class I |
| macrophages produce __, ___ and __ | reactive oxygen intermediates, nitric oxide, lysosomal enzymes |
| NK cells can be activated by | IFN-alpha, beta and IL-2 |
| __ play a role in NK activation | macrophages |
| NK cells are capable of __ killing | Fas-mediated |
| NK cells control infections during the period required for generation of | specific effector cells |
| specific effectors cells include ___ and ___ | CD4+ Th1 cells and CD8+ CTL |
| delayed type hypersensitivity is mediated by | sensitized helper T cells |
| delayed type hypersensitivity is also known as | type 4 hypersensitivity |
| roles of delayed type hypersensitivity include ___ and ___ | macrophage clearance, killing of intracellular pathogens |
| __ is a result of cytokine release and is associated with __ | delayed type hypersensitivity, tissue damage |
| effects of macrophages in CMI | killing of microbes in phagolysosomes, secretion of cytokines, increased t cell activation |
| steps to macrophage phagocytosis | attachment, ingestion, fusion, digestion, release |
| __ and __ lead to leukocyte recruitment | TNF, IL-1 |
| IL-12 leads to ___ and subsequently ____ | Th1 differentiation, IFN-gamma production |
| increased T cell activation results from increased expression of __ and ___ | B7 costimulators, MHC molecules |
| NK cells are activated by ___ and ___ dervied cytokines as early defense against intracellular ___ | interferons, macrophage, infections |
| __ (KIRs) are present on NK cells | Killer inhibitory receptors |
| KIRs recognize ___ ___ found on all host cells | self MHC I |
| when self MHC I is expressed on cell, there is | no killing |
| virally infected cells ____ the expression of ___, leading to NK killing cell | downregulate, self MHC I |
| opsonization | process by which pathogens are marked for ingestion to be recognized and eliminated by phagocytosis |
| steps to antibody dependent cell mediated cytotoxicity | antibody opsonization, NK cell FcyrIII, Activated NK cell |
| antibody opsonization leads infected target cells to express pathogen antigens on cell surface true or false | true |
| the NK cell FcyRIII receptor is also known as CD18 true or false | false, it is known as CD16 |
| FcyRIII recognize and bind to __ portion of antibodies | Fc |
| Once CD16 binding occurs | NK cell is activated |
| activated NK cells release | cytotoxic granules |
| NK cytotoxic granules either kills cells ___ or by __ | directly, FasL/Fas mediated apoptosis |
| True or False, FasL/Fas mediated apoptosis is also known as Fas induced killing | False, it is known as Fas mediated killing |
| FasL is __ of Fas | ligand |
| when cross linked, FasL/Fas trigger a ___ that leads to ___ of target cell | cascade, apoptosis |
| true or false, cytotoxic t lymphocytes are more effective and lasting in response against virally infected cells due to their specificity | true |
| CTL activation requires what 3 signals? | adhesion, antigen presentation, activation |
| CTL adhesion is generally ____ ___ to a target cell | nonspecific adhesion |
| ___ complex is presented along with ___ to activate CTL | TCR peptide:MHC complex, CD28/B7 |
| poised CTLs express high levels of ____ and low levels of __ | IL-2R beta, IL-2R alpha |
| poised CTLs secrete small amounts of __ but require additional from ___ and ___ | IL-2, Th1, CD4+ |
| IL-2R beta aka | CD122 |
| IL-2R alpha aka | p55 alpha |
| secretion of __ from CD4+ helper T cells increases __ expression leading to formation of ___ ___ IL-2R | IL-2, p55 alpha, high affinity |
| high affinity IL-2R is a __ chain structure produced on ____ cells | 3, activated T |
| during clonal expansion activated CTLs develop ___ and __ | cytoplasmic granules, cytotoxic cytokines |
| 2 possible responses to MHC I | no recognition, peptide/MHC specific recognition |
| no recognition of MHC I does not lead to ____ | killing of cell |
| pepitde/MHC specific recognition leads to | biolgical cascade and killing of cell |
| __ of T cell occurs after a CTL is activated | polarization |
| polarization of a CTL results in ___ of T cell that promote ___ formation in target cell | conformational changes, pore |
| step 1 polarization of T cells | peptide:MHC class I complex on target is recognized by TCR on CTL and stabilized by CD8 LFA-1 and ICAM-1 act as adhesion molecules |
| step 2 polarization of T cells | binding of TCR:MHC complex and adhesion molecules signals for reactivation of T-cell effector molecules towards target cell |
| step 3 polarization of T cells | reorganization of effector molecules results in delivery of lethal hit of cytotoxic granules at point of contact |
| step 4 polarization of T cells | perforins in cytotoxic granules are released in directing fashion to target cell, released perforins undergo Ca2+ dependent polymerization to form pore in target cell membrane |
| step 5 polarization of T cells | pore formation permits entry of granules that induce death by apoptosis due to influx of water |
| familial hemophagocytic lymphohistocytosis is also called | FHL |
| FHL is caused by ___ ___ of CTLs and NK cells | perforin deficiency |
| FHL means the ability to ___ __ cells is ___ | kill target, reduced |
| FHL leads to __ taking over | Fas/FasL mediated apoptosis takes over |
| opsonins | substance that binds to foreign microorganism or cells making them more susceptible to phagocytosis |
| who discovered complement | Jules Bordet |
| what are the primary synthetic sources of complement | monocytes, macrophages, hepatocytes |
| complement ___ circulate in ___ form | glycoproteins, inactive |
| 3 activation pathways | classical, alternative, lectin |
| 4 primary biological functions of complement | target lysis, opsonization of particular antigens, inflammatory response activation, immune complex clearance |
| the classical complement pathway requires __ and is activatedby ___ | antibodies, immune complexe Ag-Ab |
| classical complement pathway involves | IgM, IgG1-3 |
| alternative complement pathway is activated by __ substances | non-Ab |
| lectin pathway is an ____ process, activated by ___ | antibody independent, mannan |
| all pathways lead to production of | C5b proteins |
| activation of complement leads to | inflammation, opsonization, lysis |
| step 1 classical complement pathway | c1 complex binds to Fc receptor of antibody to target cell |
| C1 complex aka | c1qr2s2 |
| step 2 classical complement pathway | circulating C4 binds to C1q portion, r2s2 cleaves C4 into C4a and C4b |
| step 3 classical complement pathway | C4b covalently binds to cell membrane or antibody, C2 binds to C4b and C2 is cleaved in C2a and C2b |
| step 4 classical complement pathway | C4b and C2a combine to form C3 convertase |
| C3 convertase aka | C4bC2a |
| step 5 classical complement pathway | C3 converatse binds and cleaves C3 into C3a and C3b |
| step 6 classical complement pathway | C3 binds to C3 convertase to form C5 convertase |
| C5 convertase aka | C4bC2aC3b |
| what happens to unbounds C3b | either hydrolyzed or covalently bonded to target cell surface |
| step 7 classical complement pathway | C5 convertase binds and cleave C5, ending with C5b |
| mannose binding lectin (MBL) | acute phase protein produced during inflammation |
| when do steps classical and lectin complement pathways become the same | once C2 binds |
| step 1 lectin complement pathway | MBL binds to mannose residues of glycoproteins/carbohydrates on microbial surface |
| step 2 lectin complement pathway | MBL associated serine protease binds to MBL |
| MASP | MBL associated serine protease |
| step 3 lectin complement pathway | active MASP-MBL cleaves inactive C4 into C4b and C4a |
| step 4 lectin complement pathway | C4b covalently attaches to pathogen cell membrane via mannose binding and C2 binds to C4b |
| step 5 lectin complement pathway | C2 is cleaved by MASP to form C4bC2a |
| step 6 lectin complement pathway | C3 convertase binds to and cleaves c3 into C3a and C3b |
| step 7 lectin complement pathway | C3b molecules bind to C3 convertase to form C5 convertase |
| step 8 lectin complement pathway | C5 convertase binds to and cleaves C5 into C5b |
| step 1 alternative complement pathway | continuously low rate of spontaneous cleavage of C3 occurs in plasma |
| step 2 alternative complement pathway | same C3b binds to microbial surface via active thioester bond, factor B binds to c3b |
| step 3 alternative complement pathway | factor D cleaves factor B bound to c3b |
| step 4 alternative complement pathway | properdin (factor P) stabilizes C3bBb into C3 convertase |
| step 5 alternative complement pathway | additional c3 molecule is cleaved by C3 convertase |
| step 6 alternative complement pathway | binding of additional C3b forms C5 convertase |
| step 7 alternative complement pathway | c5 convertase cleaves C5 into c5b |
| classical pathway activator | ag-ab complex |
| classical and lectin C3 convertase | C4bC2a |
| classical and lectin C5 convertase | C4bC2aC3b |
| lectin pathway activator | MBL-mannose complex |
| alternative pathway activator | spontaneous hyrdolysis of c3 |
| alternative pathway C3 convertase | C3bBb |
| alternative pathway C5 convertase | C3bBbC3b |
| thioester group | R-S-CO-R' |
| what has a thioester group left bare | C3 |
| the late steps of complement activation form a pore in target cell membrane leading to its destruction, true or false | true |
| MAC equals | membrane attack complex |
| step 1 complement cascade formation of MAC | cell associated C5 convertase cleaves into C5a and C5b, C5a leaves complex |
| step 2 complement cascade formation of MAC | C6 and 7 bind to C5b, the complex is then directly instered into lipid bilayer of target cell membrane |
| step 3 complement cascade formation of MAC | C8 is bound to C7 to stabilize this complex after insertion |
| step 4 complement cascade formation of MAC | up to 15 C9 molecules polymerize to form MAC |
| complement activation is inhibited by ___ present on ___ | regulatory proteins, host cells |
| ___ and __ are inhibited by C1 inhibitor | C1r, C1s |
| C1 inhibitor aka | C1INH |
| C1 inhibitor prevents C1 complex from becoming ____ | proteolytically active |
| deficiency in C1 causes ___ | hereditary angioedema |
| HAE causes ___ and ___ | edema of skin, abdominal pain |
| Why does HAE cause abdominal pain | edema of mucosal membranes also occurs |
| c3 convertase formation can be inhibited by | decay accelerating factor, membrane cofactor protein, type 1 compement receptor |
| __ and __ act as cofactors for Factor I | MCP, CRI |
| factor I cleaves C3b to produce | iC3b and C3f |
| formation of MAC is inhbited by __ and ___ | CD59, S |
| which complement pathways are involved in the first line of defense against pathogen | lectin pathway, alternative pathway |
| why is the classical pathway activated later | activated by antibodies, needs time to develop |
| anaphylatoxins | substances produced by complement activation that causes the release of histamine and other mediators from basophils and mast cells producing anaphylaxis |
| name 3 symptoms of anaphylaxis | increased fluid secretion, peristalsis, airway constriction, increased mucous, increased blood flow/permeability |
| why are complement deficiency rarely diagnosed | redundancy in immune system |
| immune complex disease is a result of | C1, 2, 4 deficiency |
| MAC deficiency results in ___ risk of ___ | increased, infection |
| C3, Factor D and Factor I deficiencies result in | pyogenic infection |
| susceptibility to recurrent infections and decreased lung function in CF patients is a result of | MBL deficiency |
| hypersensitivity reactions are ____ ___ immune responses causing ____ effects | inappropriately exaggerated, deleterious |
| hypersensitivity reactions can possibly result in | tissue injury, serious disease, death |
| 4 type of Gell Coombs hypersensitivity reactions | immediate, cytotoxic/costimulatory, type 3, delayed |
| type 1 hypersensitivity reactions aka | immediate |
| ___ hypersensivity reactions can develop into anaphylatic responses | type 1/immediate |
| anaphylatic responses | allergic reactions that happens immediately and causes a life threatening response involving whole body |
| immediate hypersensitivity reactions are ___ ___ mediated | specific, antibody |
| ___ binds to an allergen on ____ cells, resulting in ___ | IgE, mast, degranulation |
| immediate hypersensitivity reactions can also be caused by | C3a, C4a, C5a |
| type 2 hypersensitivity reactions aka | cytotoxic/costimulatory |
| cytotoxic hypersensitivity reactions are mediated by ___ directed against cell surface antigens via ___ cells | antibody, NK |
| type 3 hypersensitivity reactions aka | immune complex |
| type 3 hypersensitivity reactions are mediated by Ab-Ag ____ ___ deposited on tissue | immune complexes |
| immune complexes on tissue activate __ and recruit ___ ___ cells to cause tissue damage | complement, innate immune |
| delayed type hypersensitivity reactions are a complex interaction of ___ and __ | t cells, monocytes/macrophages |
| allergens are generally ___ or ____ | enzymes, glycoproteins |
| 3 examples of sensitization immediate hypersensitivity reactions | oral ingestion, respiratory inhalation, skin absorption, IV |
| step 1 immediate hypersensitivity reactions | APCs present processed allergen to Th2 cells, th2 cells secrete IL-4 & 13 inducing naive B cells to undergo class switching from IgM to IgG1 to IgE |
| step 2 immediate hypersensitivity reactions | secreted IgE binds to Fc epsilon receptor on mast cell, allergen crosslinks IgE anitbodies bound to mast cell, resulting in degranulation |
| step 3 immediate hypersensitivity reactions | mast cell degranulation releases mediators which eilict biological effects within minutes |
| early phase biological effects immediate hypersensitivity reactions | histamine, eosinophil chemotactic factor, neutrophil chemotactic factor, proteases |
| histamine promotes ____ permeability and smooth muscle ____ | vascular, contraction |
| eosinophil chemotactic factor attracts ___ | eosinophils |
| neutrophil chemotactic factor attracts ___ ____ cells | polymorphic nuclear |
| proteases increase __ secretion and causes ___ __ damage | mucus, basement membrane |
| late phase biological effects immediate hypersensitivity reactions | platelet activating factor, leukotrienes, prostaglandins, brodykinin |
| platelet activating factor causes the aggregation of ___, mast cell ___ and smooth muscle ___ | platelets, degranulation, contraction |
| leukotrienes cause the same effects as __ | histamine |
| prostaglandins promote ___ ___ contraction and __ | smooth muscle, vasodilation |
| brodykinin mediates the same effects as ___ in addition to being involved in __ pathway | histamine, pain |
| vasodilation and increased blood vessel permeability can lead to __ and ___ in immediate hypersensitivity reactions | edema, anaphylatic shock |
| immediate hypersensitivity reactions can result in __ or __ on skin | uticaria, eczema |
| can also have ___ and __ in immediate hypersensitivity reactions | rhinitis, conjunctivitis |
| atopy is the ___ of developing ____ reactions | predisposition, allergic |
| asthma involves ____ narrowing and swelling | airways |
| laryngeal edema is characterized by ___ | swelling of larynx |
| atopic allergies occur in a part of body ___ __ ___ with allergen | not in contact |
| nonatopic allergies occur in a part of body __ __ with allergen | in contact |
| in cytotoxic hypersensitivity reactions, cell death occurs by | complement mediated cell lysis, phagocytosis or antibody dependent cell mediated cytotoxicity |
| cytotoxic hypersensitivity reactions are implicated in diseases where ___ ___ ___ cells are targeted | host red blood |
| in adcc antibody binds to __ region and __ binds to fc region | fab, cd16 |
| in adcc crosslinking promotes release of ___ and ___ enzymes to target cell | hydrolytic, digestive |
| the difference between adcc and phagocytosis linkage is? | phagocytic cell binds via fc region instead of cd16 |
| crosslinking enhances ___ | phagocytosis |
| ___ can also bin to receptor on phagocytic cell | C3b |
| in complement mediated lysis, antibody binds antigen forming ___ complex | ab-ag |
| complement mediated lysis ultimately results in lysis via __ | MAC |
| in hemolytic anemia, host __ are recognized as foreign | red blood cells |
| ___ ___ is a skin disease resulting in formation of blisters in space between epidermis and dermis | bullous pemphigus |
| transfusion reactions are a diverse reaction to __ red blood cells following __ ___ | allogenic, blood transfusion |
| Rh disease is a ___ condition where __ and __ blood are incompatible | hemolytic, mother, fetus |
| vasculitis | inflammation of blood vessels |
| carditis | inflammation of heart |
| pneumonitis | inflammation of lungs |
| synovitis | inflammation of synovial membrane |
| dermatitis | inflammation of skin |
| glomerulonephritis | inflammation of parts of kidney |
| optium Ag:Ab ratio results in __ complex, ___ detectable by phagocytes | large, easily |
| high Ag:Ab ratio results in __ complex, which are not as detectable and ___ in solution | smaller, remain |
| step 1 immune complex hypersensitivity reactions | antigen:antibody complexes deposit in tissue/blood vessel wall |
| step 2 immune complex hypersensitivity reactions | immune complexes activate complement and attract inflammation cells |
| step 3 immune complex hypersensitivity reactions | vasoactive amines released by basophiles will increase vascularity of tissue |
| step 4 immune complex hypersensitivity reactions | prolonged complement activation results in tissue damage due to enzymes released by neutrophils |
| arthus reaction detects __ of local __ | excess, antibodies |
| arthus reaction involves in situ formation of ___ __ after intradermal ___ ___ | immune complexes, antigen injections |
| how long does development of arthus reaction take | 6-12 hours |
| serum sickness is a reaction to __ in antiserum derived from ___ | proteins, animals |
| when does serum sickenss generally occur | after vaccination |
| farmer's lung is | hypersensitivity pneumonitis |
| rheumatoid arthritis is a longterm autoimmune disorder resulting from types __ and __ hypersensitivity reactions | 2, 3 |
| type 1 hypersensitivity reactions immune mediator | IgE |
| type 2 hypersensitivity reactions immune mediator | IgG/IgM |
| type 3 hypersensitivity reactions immune mediator | immune complexes |
| type 4 hypersensitivity reactions immune mediator | t cells |
| how long does a type 4 hypersensitivity reaction typically take | 48-72 hours |
| delayed type hypersensitivity reactions is characterized by recruitment of ____ __ to site of reaction | activated macrophages |
| effector phase of delayed type hypersensitivity reaction occurs during ___ exposure to sensitizing agent | secondary |
| delayed type hypersensitivity reaction lead to prolonged ___ to clear antigens resulting in ___ of cells | inability, aggregation |
| delayed type hypersensitivity reaction result in __ ___ after 24hrs, peaking between 48 and 72 hours | skin lesions |
| delayed type hypersensitivity skin tests are used to diagnose __ | tb |
| positive TB skin test shows | red swollen bump |
| exampled of delayed type hypersensitivity reaction | contact dermatitis |
| autoimmune diseases are a result of overreactivity of immune system against ___ ___ | own tissues |
| the presence of antiself immunity does not ___ lead to ___ disease | inevitably, autoimmune |
| autoimmune diseases can be ___ specific or ___ | organ, systemic |
| central tolerance is the mechanism by which the immune system learns to ___ between __ and ___ antigens | discriminate, self, nonself |
| peripheral tolerance is the mechanism by which body prevents ____ of immune system to various ___ factors | overreactivity, environmental |
| relative risk is the ratio of probability of an event occuring with a specific ___ to probability of the event occuring in a comparison group ___ the __ | mhc, without, mhc |
| insulin dependent diabetes is associated with specific HLA ___ haplotype | DR3/DQW8 |
| ankylosing spondylitis is associated with HLA __ hapoltype | B27 |
| 3 mechanims of autoimmune disease | molecular mimicry, release of sequestered antigen, polyclonal B cell activation |
| molecular mimicry occurs when some __ epitopes are __ to those of self antigen | foreign, similar |
| molecular mimicry may result ___ from foreign antigen and result in ___ ___ from antiself T/B cells | crossreactivity, tissue damage |
| streptococcus displays similar epitopes to those in __ and may result in ___ __ | heart, rheumatic carditis |
| multiple sclerosis is associated with | epstein barr virus, human herpes virus, milk protein butry rophilin |
| ankylosis spondylitis is associated with | klebsiella |
| where is self antigen sequestered/immunologically privileged | brain, eye lens, cornea, spermatozoa, heart muscle |
| most immature B/T cells that are self reactive are __ __ but immunologically privileged are not present during ___ therefore there is no ___ | clonally deleted, lymphocyte development, tolerance |
| if ___ or __ occur, immunologically privileged may be released and recognized as __ | infection, trauma, foreign |
| polyclonal B cell activation can cause a __ __ of cross reactivities | wide range |
| 2 types of autoimmune disease | organ specific, systemic |
| an example of neuromuscular junction autoimmune disease is | myasthenia gravis |
| myasthenia gravis is characterized by antibodies against ___ ___ ___ at neuromuscular junction | nicotinic acetylcholine receptors |
| lack of nicotinc acetylcholine receptors prevents ___ ____ | muscle contraction |
| how is myasthenia gravis treated? | it is treated with acetylcholinesterase inhibitors to prevent the breakdown of ach |
| an example of thyroid autoimmune disease is | graves disease |
| graves disease often manifests as ___ | hyperthyroidism |
| graves disease is a result of antibodies against ___ ___ ___, leading to chronic activation because it relies on __ ___ loop | thyroid stimulating hormone, negative feedback |
| grave's disease can lead to abnormally high levels of __ and __ | t3, t4 |
| graves disease generally results in __, ___ and __ | goitre, bulging eyes, muscle weakness |
| an example of kidney and lungs autoimmune disease is | good pasture's syndrome |
| good pasture's syndrome is characterized by antibodies attacking __ ___ of lung ___ and kidney___ | basement membrane, alveoli, glomerulus |
| the attacking of the basement membrane in good pasture's syndrome activates a ___ ___ | complement cascade |
| good pasture's syndrome leads to __ from lungs and kidney ___ | bleeding, failure |
| an example of DNA/RNA autoimmune disease is | systemic lupus erythematosus (SLE) |
| SLE is characterized by the body making ____ and ___ antibodies | antinuclear, anticytoplasmic |
| SLE leads to __ ___ being deposited on a variety of tissues, triggering ___ | immune complex, inflammation |
| name 3 conditions SLE can lead to | arthritis, carditis, dermatitis, vasculitis, glomerulonephritis |
| SLE is characterized by __ ___ on __ | butterfly rash, face |
| an example of a joint autoimmune disease is | rheumatoid arthritis |
| rheumatoid arthritis is characterized by _ cells engaging with a specific antigen in joints and releases ___ that initiate __ inflammation | th1, cytokines, local |
| rheumatoid arthritis is associated with ___ causing damage to __ in joints leading to its destruction | leukocytes, cartilage |
| rheumatoid arthritis involves ___ (aka rheumatoid factor), which gets deposited in __ and ___ __ | IgM anti IgG autoantibody, joints, blood vessels |
| immunodeficiency diease | defects in immune system such that the body cannot effectively fight infections or prevent disease |
| primary immunodeficiencies are caused by __/__ defect resulting in absence or improper functioning of immune system | hereditary, genetic |
| primary immunodeficiences are classified based on | what part of immune system is effected |
| 5 types of primary immunodeficiency | humoral immunity, cellular immunity, humoral and cellular immunity, phagocytes, complement proteins |
| 1/2 of primary immunodeficiency diseases are associated with | b cells |
| digeorge's syndrome is a __ deficiency | t cell |
| digeorge's syndrome is a result of a ___ deletion | 22q.11.2 |
| digeorge's syndrome causes developmental __ __ | thymic aplasia |
| thymic aplasia is the __ ___ of the thymus, meaning __ cannot mature | defective development, t cells |
| digeorge's syndrome results in anergy which is the | absence of normal immune response to a particular antigen or allergen, absence of cell mediated immunity |
| digeorge's syndrome increases suceptibility to __ and ___ infections | fungal, viral |
| bruton's agammaglobulinemia is a | b cell deficiency |
| bruton's agammaglobulinemia is also known as | x linked agammaglobulinemia |
| bruton's agammaglobulinemia is caused by a mutation in coding for ___ | bruton tyrosine kinases |
| bruton tyrosine kinases mediate development of __ __ ___ | pre b cells |
| the lack of mature b cells in bruton's agammaglobulinemia results in lack of __ in blood | Ig |
| those with bruton's agammaglobulinemia are prone to | serious bacterial infections |
| bruton's agammaglobulinemia presents similarly to | CVID/hypogammaglobulinemia |
| severe combined immunodeficiency aka | SCID or bubble boy disease |
| SCID is a | group of defects from many genes that result in inability to fight life threatening viral, bacterial or fungal infections |
| SCID causes defective antibody response one of two way, list them | mature B cell malfunctioning, ineffective T cell dependent B cell activation |
| individuals with SCID must live in a ____ | sterile environment |
| most cases of SCID are __ | x linked |
| x linked SCID is associated with a defect in gene coding for ___ __ | gamma chain |
| defect in gamma chain impacts many essential complement proteins, list 3 | IL 2, 4, 7, 9, 15 and B/T cell development |
| 4 main causes of acquired immunodeficiency | malnutrition, medication, aging and disease |
| acquire immunodeficiency is caused by some ___ __ | environmental factor |
| ___ is the most common cause of acquired immunodeficiency | malnutrition |
| malnutrition causes immunodeficiency if there are __ __ not functioning properly | 1+ nutrients |
| the most common malnutrition immunodeficiency is | protein calorie immunodeficiency |
| protein calorie immunodeficiency occurs when ___ population decreases in proportion to ___ levels | t cell, protein |
| ___ agents, such as chemotherapy, target __ ___ cells, many of which are immune cells | cytotoxic, rapidly dividing |
| ___ intentionally suppress the wholeimmune system to treat ___ or ___, increasing susceptibility to __ infections | immunosuppressant, organ transplant, autoimmune disease, opportunistic |
| the __ shrinks with age, producing fewer ___ | thymus, t cells |
| thymus shrinkage may be compounded ___ ___ | micronutrient malnutrition |
| specifically, __ and __ deficiency is common in elderly and these are essential for immune system | calcium, zinc |
| ___/___ diseases can place ___ stress on immune system causing immunodeficiency | prolonged, chronic, undue |
| the most well studied acquired immunodeficiency is | HIV/AIDS |
| HIV is a ___ stranded ___ transmitted via ___ __ | single, retrovirus, bodily fluids |
| HIV requires fusion from viral __ to ___ receptor | gp120, CD4+ TCR |
| HIV uses a ___ ___ to convert its RNA to DNA and then use an ___ to integrate its DNA into ___ genetic contents | reverse transcriptase, integrase, t cell |
| gp120 also causes CD4+ T cells to __ due to overexpression of ___ ___, on both __ and ___ t cells | apoptose, antigenic ligands, infected, uninfected |
| abnormal production of __ and ___ leads to loss of ___ __ cells | IL-1, TNF-alpha, helper T |
| the loss of helper T cells leads to decrease in ___ of t cells in response to ___ and ___ ___ hypersensitivity and ___ mediated response to _ | proliferation, antigens, delayed type, cell, infection |
| overwhelming infections in HIV leads to further ____ of ___ ___ | inhibition immune system |
| HIV also leads to other impacts on immun system, list 3 | abnormal macrophage function, decreased NK cell activation, decreased CD8+ cytotoxic T cells, increased nonspecific Ig, increased autoantibodies |
| HIV's clinical presentation begins with mild __ __ symptoms and ___ __ | flu like, generalized lymphodenopathy |
| generalized lymphodenopathy is __ ___ lymphode groups __ | 3+ noncontiguous, enlarged |
| HIV progresses to ___ ___, __ ___ cancers and death | severe infection, virus associated |
| idiopathic immunodeficiencies have _____ cause | unknown |
| Common variable hypogammaglobulinemia aka | CVID |
| CVID is associated with defects in ___ ___ region | antibody variable |
| CVID's prevalence is about ___ in those aged 15-35 | 1/17000 |
| selective IgA deficiency's prevalence in about | 1/700 |
| selective IgA deficiency cannot be treated with ___ because ____ IgA elicits ___ response | gammaglobulins, foreign, immune |
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