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IMMUNOLOGY

step one

QuestionAnswer
What kind of lymphatic organ is the lymph node secondary lymph organ
function of lymph node filtration, storage, proliferation of B&T-cells and antibody production.
Differences bet primary and secondary follicles of the lymph node primary: dense and dormant secondary: pale central germinal centers-active
Where in the lymph node are the primary and secondary follicles found follicle of cortex
where are t-cells housed in the lymph node paracortex
describe paracortex region in cell mediated immunity enlarged
described paracotex in DiGeoges's syndrome? underdeveloped
lymph vessel that drain rt. arm and rt. side of head? rt. lymphatic vessel
Lymph vessel that drains all else? thoracic duct
where are T-cells in the spleen? periarticular lymphatic sheath. (PALS)
Where are the B-cells in the spleen? within the white pulp
what is the Thymus known as? Finishing school for T-Cells. Enter immature and leave mature
what is tve selection of T-cells? signal to divide and establish clones
What is -ve selection of T-cells? signal to undergo apoptosis because of it's potential for autoimmune conditions
where in the thymus does tve and -ve selection occur? corticmedullary
what is clonal anergy? peripheral deletion that occurs to T-cells with too great affinity for self
which antigen presenting cell (APC) first react to a foreign antigen? Macrophages or any committed lymphocyte.
How does the macrophage and yet-unidentified cell acitvate THo? macrophages stimulate THo via IL-12 and yet-unidentified stimulate THo via IL-4
What is the role of the naive THo? To make a selection; CMI or humoral immunity.
To chose CMI, what is the cytokine produced? Il-12 by THo to activate Th1 of CMI
To chose humoral, what is the cytokine produced? IL-4 by THo to activate Th2 of humoral immunity
once activated, what does Th1 do? Secrete Y-INF and IL-2 to activate macrophage for independent killing.
Once activated, what does TH2 do? Secrete IL-4 and IL-5, IL-2, to stimulate B-cells to plasma cells and lymphocytes
what do plasma cells do? produce large amounts of antibodies.(ab)
how does ab mediated immunity work? defend against foreign antigen by opsonization, neutralization and complement activation
what does opsonins do? coats antigen to facilitate phagocytosis
What is the function does neutralization serve? prevention of adhesion
what is the function of the complement system? opsonize and phagocytize, and lyse infected cells
how does CMI mediate an immune attack? Via the TH1 arm of the immune pathway, resulting in cellular infiltrates like macrophages and abscess formation.
how does ab's mediate an immune attack? Via the TH2 arm of the immune pathway resulting in formation of plasma cells that result in ab prod. and ultimate opsonin, neutralization and complement activation.
eg of CMI gone awry? graft and organ transplantation rejection
eg. of Humoral immunity gone awry? allergies
What is major histocompatibility complex (MHC)? polypeptide located on cell membrane of all nucleated cells which can mediate an immune response. significant in transplantation.
how many classes of MHC have been identified? 2 classes. Class one and class 2
What do you know about MHC class I? There are 3 MHC class I gene prod, HLA A,B & C, expressed in co-dominant form. consist of 3 a heavy chain and beta 2 microglobulin light chain.
function of MHC class 1? a peptide binding groove between the 2 a heavy chain, serve to present antigen to the TCR of CD8 cells
name one cell without MHCI surface protein? RBC
what do you know about MHC classII? Also co-dominantly expressed on all APC, with 2 alpha and 2 beta components with one extra-cellular one intracellular domain. MHC classII products are HLA DP,DQ,& DR.
What is the function of MHC class II Same as Class one except it presents to the TCR of the CD4 cells.
name the types of cells that have both class I andII surface proteins on their cell membrane? All APC. macrophages, B-cells, langerhan cells and dendritic cells
Where in MHC classI does antigen loading occur? RER
Where in MHC class II does antigen loading occur? acidified endosome
describe the CD3 complex associated with TCR of T-lymphocyte and is involved in signal transduction.
When bacteria is processed and loaded in the acidified endosome, what is the next step? The loaded TCR flags the antigen on the cell membrane awaiting a TCR
once CD4's TCR commits and binds with MHC class II of APC, what happens? the CD4 secretes IL-12 to activate THo
Once CD8's TCR commits and binds with MHC classI, what happens? cell mediated killing
how does the co-stimulatory molecules of CMI work? Co-stimulatory molecule on APC B7 and C-stimulatory molecule on T-lymphocyte interact to mediate CMI
what branch of the immune system is the natural killer cell (NK)? innate
name the cell markers of NK cells CD16 $ CD 56
What is EBV's target? CD21 of B-cells
which cells mediate the immune response to HSV and EBV T-lymphocytes and NK cells
How many parts to Ig structure? fab and Fc fragments
which portion is embedded in the cell? the carboxyl terminal of the FC fragment
describe the part that is flagged by the cell and opposes the carboxyl terminal? the amino terminal
Describe the hinge region region where the Fab and FC region are held together by disulfide bonds
function of varible region of Fab fragment recognizes antigen
where would you find both heave and light chains? In the Fab fragment held by dissulfe bonds
What is the FC fragment made of? heavy chains consisting of constant regions
function of constant region of IgM and IgG? Fixes complement
what is the function of the hypervariable region of heavy & light chanis? allows for ab to have a vast number of specificities called ideotype
whcih is the better complement activator, IgM or IgG? IgM because it is a pentamer
What is the complement system? A set of interacting proteins released into the blood after production in the liver.
what is their function they serve as zymogens, participating in a cascade of reactions that culminate mediation of inflammation and lysis by MAC complex
describe initiation of complement system Initiated by the classical pathway when 2 molecules of IgG or IgM bind to C1, or the Alternate pathway.
Describe initiation of the complement pathway more primitive of the 2 pathways. initiated by attraction of early factors to surface of microbes.
Where does IgG bind to the Ab molecule? IgG binds to the Fc region by the hinge region
function of Random combination of VJ and VDJ genes for diversity
function of random combination of heavy and light chains? for diversity
define somatic diversity aka affinity mutation. mutation that occurs after antigenic contact.
function of somatic diversity? for diversity and tighter specificity of the epitope
what is terminal deoxynucleotidyl transferase Tdt? inserts bases withour template at the junction of VDJ segments randomly. All to create more diversity
which terminal illness is Tdt a marker Tdt
what 2 Ig do mature B-cells express? IgM and IgD
what is isotype switching? switching from IgG to IgA to IgE
who mediates isotype switching? cytokines and CD40L
which other cell produce different isotypes plasma cells but does not switch only makes the isotype for which it is cloned.
name the ab in a primary response IgM
Describe IgM a monomer in tissue, pentamer in blood, tve on mature B-cell andfixes complement. No placental access
name ab in a secondary response? IgG
Describe IgG most abundant Ig, fixes complement, good opsonin, neutralizes bacteria, and crosses the placental barrier.
how does IgA work to fight infection? found in secretions that line the mucosa, picks up secretory component from epithelial cells before secretion prevents attachment of bacteria to mucosa.
function of IgD? unclear. Found on the surface of mature B-cells and in serum.
functions of IgE mediate immediate immune response, ie type one hypersensitivity and immunity to helmithic infection.
how does IgE mediate it's type of immunity? induces the release of mediators from mast cells, basopils and eosinophils when Ig is stimulated by the exposure to allergens
define allotype immunologic epitope that is different among members of the same species. may be heavy or light chain. Allotype determines compatibility for transplant.
define isotype immunological epitope common to a single class of Ig. ie IgG, IgA. determined by heavy chain.
define ideotype Ig epitope, determined by antigen binding site.
define hapten small, single antigenic determinants, unable to mount an immune response independently but can if coupled with another protein.
name ex. of hapten meds like asa, streptomycin, sulfa, some opiates, like morphine.
mneumonic for remembering function of IL-1 and IL-2. HOT T-bone sTEAK IL-1 -pyrogen, IL-2 - increased T-cells, IL-3 -increased bone marrow , IL-4 - IgE, IL-5 -IgA.
function of IL-1 endogenous pyorogen, stimulates B & T-cells, nuetrophils, fibroblast, & epithelial cells to grow and differntiate or synthethize prod.
function of IL-2 secreted Th cells and stimulates growth of Th and Tc cells.
function of IL-3 similar function of GM-CSF, secreted by activated T-cells. Increase growth and differentiation of BM stem cells.
function of IL-4 secreted by B-cells, enhances class switching from IgG to IgA, and production and activation of eosinophils.
function of IL-8 major chemotactic stimuli for PMN's
function of IL-6 stimulated by Th cells and macrophages. stimulates prod. of acute phase reactants and Ig's
function of IL-10 secreted by Th2, stimulates Th2 while inhibiting Th1. Encourages humoral immunity while inhibiting cellular.
function of IL-12 secreted by B-cells, naive cells and macrophages and activates NK and Th1. CMI
function of Y-interferon secreted by Th1 cells destroys viral infected cells.
function of TNF alpha secreted by macrophages, increases IL-2 receptor synthesis by Th cells and increases B-cell proliferation. chemotactic to PMN's
list surface markers of T-helper cell CD4, TCR, CD3, CD28, CD40
list surface markers of T-cytotoxic cell CD8, TCR, CD3
cell surface marker for B-cell IgD, IgM, B7, CD19, CD20, CD21,CD40L, MHCII
cell surface protein of macrophages MHCII, MHCI, CD14, FC, C3b
cell surface protein of NK cells MHCII, CD16, CD56
cell surface markers for all cells x RBC MHCI
function of TCR antigenic recognition
function of CD40L class switching
function of CD3 signal transduction by TCR
function of CD28 Tcell receptor for co-stimulatory signal with B7
function of CD19 co-receptor with B21 for signal activation transduction
function of CD20 unknown role in Bcell activation
function of CD21 receptor for complement fragment C3D, CD21, and for EBV
function of C3b opsonin
Another opsonin IgG
function of B7 APC receptor for co-stimulatory molecule B7
function of CD14 on monocytes, macrophages and PMN's which binds LPS. Receptor of superantigens
function of CD16 opsonization, ADCC
function of CD56 unknown
IL-1 & IL-2 are both endogenous pyrogens. why is that good for infection? creates harsh environment for growth, causes rt. shift of oxy/Hg curve making Hg for O2 making it available for the oxygen burs kill.
What is the complement system system of proteins which interact and break into split products to fight infection, mediates humoral immunity and inflammation.
how many limbs are there to the complement system 2 pathways: classic and alternate
how is the classical pathway initiated? IgG and IgM
how is the alternate pathway initiated? by reaction of the more primitive split products to the manose-lethicin membrane of bacteria's cell membrane
function of the complement system mediate inflammation, opsonization and lysis
mneumonic for classic pathway GM makes classic cars. (IgG & IgG initiates the classic pathway
Name the 1st split product to be produced C1
Where does C1 bind to the Ig to initiate the System? clsoe to the hinge region in the FC fragment
function of c3b opsonization
function of c1, c2, c3, c4 viral
function of c3a, c5a anaphylaxsis
function of c5a neutrophil chemotaxsis
function of c5b - 9 mac complex
why is IgM a more effective activator than IgG IgM is a pentamer and can bind x5 more than IgM which is a monomer.
result of C1 esterase deficiency overactive complement due to loss of inhibitory enzyme.
clinical presentation of c1 esterase defeciency angioedema
clinical presentation of c3 deficiency severe, recurrent, pyrogenic, sinus and resp infections.
clinical presentation of c6 and c8 deficiency Neisseria bacteremia
what is decay accelerating factor? regulatory protein of complement.
role of INF to uninfected cells? Places all cells in an antiviral state.
what antiviral process does INF induce? it produces a protein that degrades viral RNA, but not host's.
how does INF alpha and gamma fight infection? Increases MHCI and MHCII expression on all cells.
how does INF affect NK cells? activate Nk cells to kill viral infected cells
how does INF enhance CMI? mediates ADCC: ab dependent cell mediated cytotoxicity.
what kind of immunity is achieved by HBV, botulinum toxin etc? artificial, passive
what kind of immunity is achieved by DTaP? artificial, active
is passive immunity slow onset with memory? No! Rapid and short term with no memory.
Hiv+ mom gives birth to baby who is sero- at 6 months. What kind of immunity is this an example of? passive
define antigenic variation? process of varying antigenic proteins to hide from the onslaught of the immune system.
describe 2 mechanism for antigenic variation 1. DNA rearrangement 2. RNA segment resortment
an example of RNA segment reasortment H. influenza
Describe salmonella's mechanism of antigenic variation 2 flagella variants
describe the result of Borellia's mechanism of antigenic varaition. relapsing fever.
Describe Neisseia gonorrhea's mechanism of antigenic variation pilus protein
mneumonic for shift and drift antigenic shift -fast - epidemics.antigenic drift- slow - pandemic.
define anergy Ocurrs to self reactive T-cells in the periphery of the thymus. Undergoes apoptosis.
does B-cells undergo anergy? yes, but tolerence is less complete than with T-cells.
When the T-cell emerges from the BM is it mature? No, it is immature and naieve with CD4 and CD8 cell srface makrers.
when is the T-cell matured? After it has made a commitment to carry either CD$ or CD8
How does a T-cell show committment A CD4 T-cell with low affinity for class II receptors or CD8 T-cell with low affinity for class I .
What if it has high affinity for its own class? The the cell line experiences - selection. If not, + selection.
Explain how PPD works Activates Th1 to mediate a CMI response to the mycobacteria tuberculosis antigen.
Does encapsulated organisms demonstrate antigenic variation? No. what they do is directly activate macrophages and T-lymphocytes to release mediate an exaggerated inflammatory response leading to septic shock syndrome.
Name the receptor on the macrophage that bind with the APC CD14
What type of sensitivity is first and fast? Type 1 hypersensitivity
name an example of Type 1 hypersensitivity anaphylaxsis
How does this occur? Throughthe release of vasoactive amine from the binding of antigen with preformed ab.
What is type II hypersensitivity? Cy-2-toxic. Classical pathway activated by IgM and IgG, which binds wit ab to start the omplement system.
name examples of type II hypersensitivity autoimmune hemolytic dz, HDNB, Good Pastures,RF, Graves dz, Billous Pemphigoid, MS, & ITP
What is type III hypersensitivity? antigen/ab/complement complex which induces PMN's to the area, that releases its lysosomal enzymes causing tissue distruction.
name examples of type III hypersensitivity PAN, immune complex glomerulonephritis, RA, SLE.
describe how serum sickness fits into the category of type III hypersensitivity. ag/ab complexes, five days post exposure release complement that mediate tissue destruction.
clinical presentation of serum sickness fever, uticaria, arthralgias, proteinemia, lymphadenopathy, 5-10 days post exposure.
How is arthrus formation type III hypersensitivity? via local injection of antigen, where an ag/ab/complement complex forms.
example of dz causig arthrus formation Farmaers lung- hypersensitivity pneumonitis and thermophilic actinomycetes.
define type IV hypersensitivity T-cell mediated. Once sensitized T-cells release lymphokines once antigen is encountered
Is the reaction immediate? No, clinical presentation is delayed and occurs contact with the antigen.
In latex allergy, which hypersensitivity is in effect? Depends on the onset of sysptoms. I immediate-Type I, If delayed-type II.
Nmae the 4 T's of type IV hypersensitivity. T-lymphocytes, Transplant rejection, TB skin test, Touching-contact dermatitis like poison ivy.
mnuemonic for hypersensitivity. Anaphalactic and atrophic -I, cytotoxic, ab mediated - II, immune complex complement -III, Delayed -IV. ACID
what is Burton's agammglobinemia? X-linked recessive, decreased production of B-cells.
why are T-cells deficient in De-George's syndrome? Thymic aplasia - underdeveloped thymus
Embyrogenic origin of thymus and parathyroid? 3rd and 4th phryngeal pouch.
complications of DeGeorge's Tetany due to hypocalcemia, recurrent viral and fungal infections, T-cell deficiency and congenital defects.
name location of genetic defects? 22q11 deletion defect
describe B&T cells combined immune deficiency.SCID defect-early stem cell differentiation. Recrrent bacterial, fungal,protozoal infection to opportunistic illness.
Cause of SCID? multiple causes but most frequent is adenosine deaminase degiciency.
other causes of SCID? IL-2 receptor impairement and failure to synthesize MHC II antigens
What dz presents with disseminated mycobacterial infections? T-cell IL-2 deficiency.
defects on CD40L on T-cells causes what dz? hyper IgM syndrome with decreased class switching and loss of humoral limb.
clinical presentation of hyperIgM. overactive CMI- pyogenic infections. Elevated serum IgM and decreased IgE, IgG & IgA.
what is Wiskott-Aldrich syndrome? X-inked defect causing an inability to mount an IgM response to capsular polysaccharide of bacteria.
How does serum levels of Ig present in wiskott-Aldrich syndrome? IgE - normal and low IgM
Wiskott-Aldrich's presentation WIPE: with pyogenic infections, purpura(thrombocytopenic), and Eczema
What is Job's syndrome? Failure of INF-gamma production of T-helper cells so PMN's has no chemotactic stimulation
how does job's syndrome present retained primary teeth, recurrent colds, and staph abscess, eczema and coarse features.
Serum level in Job's syndrome? Increased levels of IgE
Diagnosis of B and T-cell defficiences is by what? Flow cytometry
How would LAD present? Severe, recurrent and fungal infection with delayed separation of umbilicus.
How would LAD present on flow cytometry? negative CD18 expression
What is cheiak Higashi? autosomal recessive defect in microtubular function and lysosmal emptying of phagocytic cell
presentation of Chediak Higashi? recurrent pyogenic infection with taph,strep, partial albinism and peripheral neuropathy
what is CGD defect in phagocytosis of PMN's secondaryto lack of NADPH oxidase activity.
presentation of CGD recurrent bacterial, viral and fungal infections.
Name infection commonly seen in GCD mmmmmmn
how is DX confirmed? negative nitroblue tetrozolium dye reduction test is indicative of a t dx.
All dysfunction of T-cells presents as skin and mucosal membrane candida infections
All dysfunction of B-cells would presents as deficiency in a specific clas of imunoglobulin.
common causes of B-cell deficiency defective isotype switching
wich Ig is frequently deficient? IgA
how does IgA deficiency present? sinus and lung infections. associated with milk allergies and diarrhea.
What is B-cell ataxia telangectasia? Defecet is in DNA repair enzymes with associated IgA deficiency
how else will telangectasia present? cerebellar problems. ataxia and spider angiomas aka telangectasia.
many autoimmune dz pesent with elevated levels of ab titers
SLE increased ANA (antinuclear)
AB that are specific to SLE anti-ds DNA, antismith
what kind of lupus presents with high levels of antihistone? drug induced SLE
Rhumatoid arthritis Rhumatiod factor- anti-igG
vasculitis antineutrophils, C-ANCA, P-ANCA
scleroderma (CREST) anticentromere
scleroderma (diffuse) anti-scl-70
primary billary cirrhoses antimitochrondrial (AST/ALT)
celiac dz antigliadin
Good Pasture syndrome antibasement membrane
pemphigus vulgaris antiepithelial
Hashimotor thyroiditis antimicrosomal
Name infection commonly seen in GCD mmmmmmn
how is DX confirmed? negative nitroblue tetrozolium dye reduction test is indicative of a t dx.
All dysfunction of T-cells presents as skin and mucosal membrane candida infections
All dysfunction of B-cells would presents as deficiency in a specific clas of imunoglobulin.
common causes of B-cell deficiency defective isotype switching
wich Ig is frequently deficient? IgA
how does IgA deficiency present? sinus and lung infections. associated with milk allergies and diarrhea.
What is B-cell ataxia telangectasia? Defecet is in DNA repair enzymes with associated IgA deficiency
how else will telangectasia present? cerebellar problems. ataxia and spider angiomas aka telangectasia.
many autoimmune dz pesent with elevated levels of ab titers
SLE increased ANA (antinuclear)
AB that are specific to SLE anti-ds DNA, antismith
what kind of lupus presents with high levels of antihistone? drug induced SLE
Rhumatoid arthritis Rhumatiod factor- anti-igG
vasculitis antineutrophils, C-ANCA, P-ANCA
scleroderma (CREST) anticentromere
scleroderma (diffuse) anti-scl-70
primary billary cirrhoses antimitochrondrial (AST/ALT)
celiac dz antigliadin
Good Pasture syndrome antibasement membrane
pemphigus vulgaris antiepithelial
Hashimotor thyroiditis
polymyositis dermatomyositis antijo-1
What cell surface protein show a prediliction for certain diseases. HLA subtypes
psoriasis, ankylosing spondylitis, IBS, Reiters syndrome show a prediliction for HLA types B27
Graves dz. celiac sprue HLA types B8
MS, hay fever, SLE, Goodpastures DR2
DM1 DR3
DM2, Rhumatoid arthritis DR4
pernicious anemia, B12 deficiency, Hashimotor thyroiditis. DR5
Steriod sensitive nephrotic syndrome DR7
Occurs in minutes ue to preformed ab in transplant recipient against donor antigen hyperacute rejection
occurs weeks after transplant from T-cell response to foreign antigen acute rejection
is acute or hyperacute rejection reversible? Hyperacute NO! acute Yes!
occurs months or years after transplant with ab-mediated vascular damage -fibrinoid necrosis chronic rejection
is chronic rejection reversible? No! but controlled with steriods/ antirejection
What is graft vs host dz? Grafted Immunocompetent T-cells proliferate in the irradiated immunocompromised host and mount an immune response
presentation of Graft vs host dz hepatosplenomegaly, maculopapular rash and diarrhea. Triad
sequale of graft vs ost dz severe organ dysfunction
what is an autograph? donor is same individual
synergenic? donor is an identical twin
allogenic? donor is genetically different member of same species
xenogenic donor is from another species
what type os dz is an exlusively B-lymphocyte mechanism class switching - humoral division
genetic difference of aa in heavy/light chains and have no biologic significance. allotypic variation
Created by: mavis41