Immunology terms and Concepts
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| Atopy | Allergy causing
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| Anergy | From immature B cell binding soluble self antigen in 1st 12-24 hrs of B cell life
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| Apoptosis (immature B cells) | From binding self antigen on cells in bone marrow
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| Signal Joint | Circular discarded
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| Coding Joint | Linear transcribed
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| Hypervariable Regions | 1st 2 gene encoded, third from PNP region between VJ
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| Ig Transcription regulation | Promoter and enhancer are brought closer by V-J recomb
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| Recombination signal sequence (RSS) | 12-23 rule
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| Alloreactivity types | Peptide Dominant and MHC Dominant binding
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| Superantigens | Elicit broad T cell response to all those T cell receptors expressing particular Vbeta regions (14 different types) Staphylococcal enterotoxin, toxic shock syndrome toxin (TSST-1) Mammary tumor virus (MMTV-7)
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| Allelic Exclusion | If first chromasome's V-DJ rearrangement is productive, other chromasome doesn’t rearrange
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| Receptor Editing | When immature B cell binds self antigen, RAG1/2 reactivate and recombine light chain again to try to get cell that won't bind self antigen
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| Germinal Center | Focus of Proliferating B cells which have been helped by CD4 T cells (region inside primary follicle of lymph node)
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| T Cell Selection in thymus | Positive Selection by cortical epithelial cells; Negative selection by dendritic cells
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| 2 Signals for B cell Activation | Antigen binding and signalling cascade; and Th2 cell stimulation--cytokines and CD40:CD40 ligand interaction and production of cytokines IL-4,5,6 (for Thymus dependent antigens)
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| Linked Recognition | TD antibody responses require activation of B-cells by Th2 cells that respond to SAME antigen (B cell being the APC expressing MHC II for Th2 guarentees this)
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| Hapten & Carrier | Epitope of antigen recognized by B cells (binds Ig); Epitope of same antigen recognized by Th2 cells; Haptens are antigenic (stimulate 1st B cell signal) but not immunogenic b/c they lack component of antigen recognized by Th2 (carrier)
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| Hyper IgM Sydrome | 2 Types: Type I--failure of T cells to produce CD40 Ligand; Type II--deficiency of AID (no somatic hypermutation or isotype switching)
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| Follicular Lymphoma | Gene translocation results in BCL-2 family proteins (anti-apoptotic) constitiutively upregulated--B cells never die
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| Primary Response | IgM
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| Anamnestic Response | IgG, IgA, IgE
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| Thymus Independent antigens | Stimulate B cells in absence of Th2 cells. Do NOT activate T cells. Usually parts of common bacterial cell walls--e.g. LPS; 2 types:
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| TI1 antigens | bind specific receptors on B cells. usually polycolonal activators at high concentration like B cell mitogen or LPS. Antigenically specific at low conc.
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| TI2 antigens | highly polymeric structures e.g. polysaccharides or polymeric peptides--Main response is by B1-B cells and thus not Somatic hypermutation or isotype switching (IgM only) and no memory cells
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| Hygiene Hypothesis | "The cleaner we get, the more allergic we become"
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| Perinatal Immunodeficiency | Half life of IgG from placenta ~ 3wks. IgM low for 1st 6 mo. Normal self IgG/IgA not unil 3-5yrs. In absence of other Ig (e.g. IgA in breast milk) there is a normal period (~4 yrs) or immunodeficiency where children are particularly susceptible.
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| Complement Pathways | are essential for phagocytizing an organism with a protective mucoid coat (FYI)
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| Classical Pathway | Only pathway involving component of acquired immune system (IgM or 2IgG) binds C1qrs--therefore has a lag phase while Ig is genereated
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| Alternative Pathway | makes soluble C3 convertase iC3Bb to place C3b fragment on microbe surface
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| Lectin Pathway | Mannose-binding lectin (MBL and associated serine proteases (MASP-1,2,3) recognize mannose patterns and activate classical C4b2a convertase and then continues through amplification loop like other pathways
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| Chronic Myelogenous Leukemia (CML) | Philadelphia chromasome transloc. Hyperprolif. of B cells d/t constitutive express. of bcl-2 gene family-->VERY HIGH WBC#s, fatigue, bruising&clotting problems, anemia (low Hb), hepatosplenomegaly & marrow packed w/ myeloid lymphocytes
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| HANE | Hereditary Angioneurotic Edema--reduced levels of C1INH--hyperreaction of anaphlatoxins causing edema--triggered by stress--results finally in C3b being totally depleted.
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| Extracellular infection (fluids/interstitial spaces) | Protect via Ab's, complement, and phagocytosis
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| Epithelial infection | Protect via IgA and antimicrobial peptides
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| Cytoplasmic infection | Protect via CD8 T cells and NK cells
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| Vesicular infection | Protect via activating macrophages containing infected vesicles
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| Commensal bacteria | normally present protective bacteria in gut--killed off during antibiotic tx.--makes susceptibe to opportunistic infection like clostridium difficile
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| Glomerular Nephritis | can be caused by Immune complexes of antigen:antibody:complement binding Fc receptors-->clogs up the glomerular capillaries, then falls apart and results in tons of antigen present in kidney
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| Immune Complexes | cleared by binding erythrocyte CR1 receptors and being carried to spleen and liver, where macrophages and kupffer cells can remove complexes and degrade.
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| Acute Phase Response to infection | by IL-1, IL-6, TNF-α. Liver (IL-6)--makes acute phase proteins (C-reactive p., MBP) for complement; Marrow mobilization of neutrophils; Hypothalamus, Muscle and Fat promote fever; Dendritic cells stimulated by TNF-α go to mature lymph nodes.
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| Response to primary Immunization | IgM takes lion's share and IgG doesn't show up until later
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| Ab Response to secondary immunization | IgG increases significantly because through memory it has gotten better and binding antigen via affinity maturation. Now little effect of IgM
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| Cytokines Promoting memory T cell production | IL-7R, IL-15R, and some anti-apoptotic molecules
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| Cytokines Promoting effector T cell production | , IL-4
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| Original Antigenic Sin | Only first infection yields cell memory. Subsequent infection w/ any epitopes shared w/ original infection cause antibody memory response for only ones common with memory epitopes. Thus primary infection only occurs w/ a completely novel set of epitopes
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| Type I Hypersensitivity | IgE Mediated --triggers mast cell degranulation--can range from Hay Fever to Systemic Anaphylaxis--Itching is always an indicator of Type I
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| Type II Hypersensitivity | Antibody Mediated (non IgE)--involves IgG binding either cell surface receptor or complement and FcR+ cells--e.g. drug allergies and urticaria (hives) and Blood transfusion type reactions
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| Type III Hypersensitivity | Large antigen presence-->continued production of IgG binds antigen---> Immune Complexes to be phagocytized, but if IgG given in large bolus, can overwhelm the phagocytic ability of macrophages in liver & spleen. Anaphlatoxins cause inflamm.& tissue damage
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| Type IV Hypersensitivity | Cell Mediated --T cells overactivated cause contact dermatitis, chronic asthma, tuberculin reaction, etc. Delayed type w/ insect venom, Contact type w/ poison ivy or metals, or Gluten sensitive-->Celiac disease (villous atrophy in sm. bowell & malnutrit.
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| Anaphylactic Reaction Characteristis | Type I Systemic IgE reaction***Very important is extreme anxiety, as well as wheezing and inability to EXHALE. Also rapid and severe drop in blood pressure. Treat with immediate epinepherine as well as bicarb
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| Anaphylactic exposures | First exposure immunizes to antigen--. Subsequent exposures then possibly elicit anaphylaxis (Type I reaction)
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| Eosinophilia | originally a Type I reaction used to get rid of parasites--involves toxic remodeling of CT, neurotoxins, mast cell response, chemoattractants and amplifiers
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| Hemolytic Disease of the newborn | Mom Rh-. 1st pregnancy: fetus Rh+, @ birth fetal blood gets in mom's circulation--she builds anti-Rh Ab. Subsequent pregnancies: Maternal anti-Rh IgG crosses placenta, binds fetal RBCsRh, & macrophage receptor binds IgG causing phagocytosis (no complement
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| Prevention Hemolytic newborn disease | Before 1st birth and before all subsequent births of Rh+ babies, Rhogam (anti-Rh Ab) is administered to mother which prevents any progression to memory immunity for Rh. Anti-Rh Ab must be given to mother on EACH subsequent birth as well.
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| Anaphylactoid Reaction | Looks like anaphylaxis b/c mechanism can't be tied directly to IgE. E.g. IV morphine is a direct decragnulating agent of mast cells--NOT true allergy
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| Anaphylaxis Differential | Vasovagal collapse, Hyperventilation, Arrhythmmias, MI, Aspiration of Food, PE, Seizures
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| Anaphylaxis Treament | Secure airway--intubate or trache if necc. EPI 1:1000 subQ--.01ml/kg, max .3 to .5; Repeat q15min. Tourniquet if able, if worsening, O2 and IV to raise BP, corticosteroids can only help if given some time. Norepi is last ditch effort if all else fail.
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| Atopic Dermatitis | (Eczema) often from late phase food allergy--esp. in young; as people tend to lose allergies as they age
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| Contact Dermatitis | Type 4 hypersensitivity--indistinguishable from ezcema--regular skin tests won't show. Have to do longer term patch test.
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| Urticaria | (Hives) Type 1 hypersensitivity reaction--hives itch and move around
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| Erytheyma multiformi | Type III hypersensitivity reaction--from e.g. drugs--doesn't itch and stays in the same place
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| Stephen-Johnson's Syndrome | Type III hypersensitivity reaction with a component of Type IV--starts with Erytheyma multiformi, then moves to eyes, then skin starts to come off--often from drug reaction (e.g. bactrin, acetaminophen or dilantin). Skin tests are worthless
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| Skin Allergy test pitfalls | Only reacts if Type I allery. Drugs Like antihistamines, amitriptylline or imipramine (tricyclic antidepressants) tend to inhibit skin Type I reaction--must know if on these
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| Allergic Rhinitis | Type II hypersensitivity reaction--sees eosinophils in the nose
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| Asthma | Type I or IV hypersensitivity reaction--3 components: Airway wall edema, Smooth muscle constriction and mucosal secretion
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| Primary/Secondary Immunodeficienies | Primary/Secondary Immunodeficienies
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| Wiscott-Aldrich Syndrome | Sign of immunodeficiency of this type is small platelets; Eczema with little spots of blood in skin (petichiae) b/c platelets not working right
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| DiGeorge Syndrome | T-Cell deficiency: Characteristic facial qualities--Prince Charles ears, puckered fish mouth; as well as congenital heart defects--caused by branchial cleft malformation results in never forming a thymus and parathyroid glands (--->calcium deficiencies)
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| Chronic Mucocutaneous candidiasis | T-Cell deficiency: Only lack T cell clone to fight of candida (yeast) comprehensive yeast infection of skin, nails, and face
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| SCID | Severe Combined Immunodeficiency--lack both B & T cells--due to Adenosine Deaminase deficinecy
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| Hyper IgE syndrome | Combined B&T cell deficiency---characteristic coarse face, broad eyes and thicker lips--get pneumatoceles (abcesses in the lung) and other abcesses
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| Common Variable Immune Deficiency | Both B&T cell defects make no functional Ab and often have autoimmunity conditions
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| Ataxia Telangeiectasia | Both B&T cell deficiency with Bloodshot scleral capillaries & lack of trunk control-->can't walk, then later develops immune deficiency
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| Immunodeficency before and after 6 months old | T cell and B cell deficiencies, respectively
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| X- Linked Agammaglobulinemia | from inability to express Btk--can't make Ig b/c B cells get no further than preB cells) in boys only b/c recessive
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| IgG Deficiency | No sublass 2&4. e.g. kid who can't fight H. influenzae
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| IgA Deficinecy | B cell deficinecy--most common--Sinopulmonary infections, asthma, brochitis. Bronchiectasis--permanent damage to brochi making more susceptible to infection
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| Specific Anitbody Deficiency | B cell deficiency that makes Ig ok, but when vaccinated, pt. doesn’t mount a response
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| Transient Ig Deficiency of Infancy | Ig very low @ 6 monthes, but functional--tends to correct ~3-5 yrs.
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| Phagocytic Deficiencies | low grade bacterial virulent infections - e.g. E. coli, skin infections and abcesses, and delayed separation of umbilical cord, Extremely high blood neutrophils but none in infections b/c adhesion problems
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| Chronic Granulomatous Disease (CGD) | Phagocytic (deficient Ox. metabolism) disorder, classic present. for neutrophil disorder--lymphadenop, hepatomegaly, infected lungs, & infection pre-2 y.o.--get granulomas--many uncommon infections: aspergillis or norcardia (in dirt), salmonella, serratia
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| Labs for Phagocytic disorders | NBT, Dihydrorhodamine test (CGD), CBC White count w/ diff, Flow cytometry for adhesion markers, Boyden chamber for actin problems
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| Complement Deficiency | C3 deficiency-->recurrent Bacterial infections; C5,6,7,8 deficiency-->common Neisseria gonococcal infections
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| Methods of Peripheral Tolerance of T cells | Lack B7 costimulation, failure to encounter self antigens, Fas:Fas ligand, regulator T cells
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| Methods of Peripheral Tolerance of B cells | Encounter of self antigen renders anergic. CD4 T-cell later encounters and signals for apoptosis through FasL:Fas
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| Autoimmune hemolytic anemia | Type II autoimmune disease mediated by Ab specific for Rh group antigens and leads to destruction of RBCs (thus anemia) by complement and phagocytes
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| Autoimmune thrombocytopenia | Type II autoimmune disease mediated by Ab specific for a platelet protein and leads to bleeding problems
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| Acute rheumatic fever | Type II autoimmune disease mediated by Ab specific for streptococci, but also react with cardiac muscle; causing arthritis, myocarditis, and heart valve scarring
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| Graves Disease | Type II autoimmune disease mediated by Ab specific for TSH receptor; leading to hyperthyroidism
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| Myasthenia gravis | Type II autoimmune disease mediated by Ab specific for Ach receptor leading to progressive weakness
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| Diabetes mellitus type II | Type II autoimmune disease mediated by Ab specific for insulin receptor agonists leading to hyperglycemia and ketoacidosis
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| Subacute bacterial endocarditis | Type III autoimmune disease mediated by immune complexes of bacteria that lead to glomerulonephritis
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| Mixed Essential Cryoglobulinemia | Type III autoimmune disease mediated by immune complexes of Rheumatoid factor that causes systemic vasculitis
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| Systemic Lupus erythematous | Type III autoimmune disease mediated by immune complexes of DNA, histones ribosomes, or other nuclear machinery that lead to glomerulonephritis, vasculitis, arthritis, and multiple system failure
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| Diabetes mellitus type I | Type IV autoimmune disease mediated by effector T cells attacking and destroying insulin-secreting pancreatic beta cells
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| Rheumatoid Arthritis | Type IV autoimmune disease mediated by effector T cells attacking antigens in synovial joints leading to inflammation and destruction. Anti-TNF-α been shown to reduce inflammation.
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| Multiple Sclerosis | Type IV autoimmune disease mediated by effector T cells attacking myelin basic protein leading to brain degeneration and paralysis
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| Celiac Disease | (Gluten enterropathy) Type IV autoimmune disease mediated by effector T cells attacking gluten on the gut tissue and damaging intestinal villi leading to malabsorption of nutrients
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| Genetics of Autoimmunity | The HLA complex of genes are strongly associated w/ susceptibility or protection from autoimmune diseases (calculated via Relative Risk) depending on serotype expressed.
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| Markers and factors Important for Blood Marrow Transplant donor | Include Class I HLA-A and HLA-B, and Class II HLA-DR (all 3 inherited via a common cassete; Crossmatching RBCs, HLA-DR/DQ typing, viral titers (esp. CMV), and organ functions (e.g. LFTs or Creatinine)
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| Cytomegalovirus (CMV) | Benign viral infection normally. As much as 50% of poplulation infected or carriers. Normal people affected are asymptomatic. However, a CMV infection in an immunocompromised Pt. like marrow recipient can be catastrophic.
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| Autologous type Bone Marrow Transplant | Takes marrow from self--No chance of GVHD or Graft versus tumor Effect
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| Allogeneic-type Bone Marrow Transplant | Takes marrow from matched donor (related or no)--risks GVHD and also gets Graft versus Tumor effect
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| Syngeneic and Xenogeneic-types of Bone Marrow Transplant | Syngeneic and Xenogeneic-types of Bone Marrow Transplant
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| Checking CD34 on progenitor cells on donor marrow cells | Marker seen in very young and pluripotent stem cells--asseses quality of marrow donation.
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| Management of Post-Marrow Transplant Patients | Immunosuppressants to prevent GVHD (e.g. Cyclosporine and Methotrexate), platelet transfusions,
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| Acute GVHD | Seen within 3 mo. Usually see maculopapular skin rash (***often on palms of hands & feet), Liver damage (rising bilirubin), & GI effects (diarrhea). Diagnose by liver biopsy & treat w/steroids (e.g. methlyprednisolone) & continued cyclosporine
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| Chronic GVHD | After 3 months--still effects skin, liver and GI. But sypmptoms vary--subsets of lymphocytes within body reacting to various host tissues. Also expecially susceptible @ this point to infection-->prophylaxis w/ Bactrim, Penicillin, &IVIG
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| Post Bone Marrow Late phase infections | Resulting from impaired cellular and humoral immunity (immunosuppression from cyclosporine) include Pneumocystis carinii, Varicella Zoster, and various encapsulated bacteria.
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| Restriction Fragment Length Polymorphism (RFLP) analysis | Pre transplant ID of DNA markers characteristic to donor & to recipient. Post transplant comparison of recipient markers will (ideally) be identical to the characteristics of donor (fully engraphed). Relapse indicated by persistent post-op patient DNA.
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| Relapsed CML course of action | Try Donor Lymphocyte Infusion (not whole marrow). DLI can often fight CML lymphocytes and result in remission (though DLI can result in death, or marrow aplasia). If Not, consider another BMT
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| Hematopoetic cytokines (differentiation to neutrophils | GM-CSF (throughout), IL-3 (early on--e.g. myeloid stem cell), and G-CSF (later and end stages)
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| Cytokines used to enhance function of monocytes/PMNs | G-CSF & GM-CSF (Neulasta/Neupogen--can renew granulocytes in Pts. w/ solid tumors after chemo); as well as M-CSF
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| Mobilization of hematopoetic stem cells for transplant | G-CSF not only promotes maturation and differentiation of stem cells, but also can promotes migration of stem cells directly into blood from bone marrow w/out maturing
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| Normal White count in blood and Tx for excess or lymphocyte harvesting | 4000-12000. White count upwards of 70000 becomes problematic--possible overkill w/ G-CSF--use plasmaphoresis to remove interphase layer to get white cells & stem cells out. CD34 count of harvest indicates concentration of stem cells harvested
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| Clinical uses of cytokine EPO | For anemic patients d/t chronic renal failure (b/c EPO normally made in kidneys) or pre-leukemia (myelodysplastic syndrome)
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| Theraputic uses of IL-2 | In Renal cell carcinoma or melanoma to fight cancer. Regulates lymphocyte activation, growth, & differentiation--Autocrine growth factor for T-cells & Enhancing NK cell activity. Side FX include Vascular Leak Syndrome & induction of inflamm. cytokines
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| Theraputic uses of IFN-α | Promotes innate immunity & resistance to viruses; antiproliferative (for CML or multiple myeloma)--anti-angiogenesis and anti-tumor. Most people develop flu-like symptoms, myalgias, tachycardia, headache and fatigue
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| Theraputic uses of IFN-γ | Not used frequently. Activates nonspecific effector cells. Normally from CD4 Th1 cells and CD8 T cells. Induces enzymes to enhance respiratory burst (e.g. macrophages & neutrophils). Useful for CGD (deficient oxidatvie metabolism)
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| Virus Attenuation | Isolate virus from infected human, grow in culture, infect monkey. Virus growing in monkey mutates to form unviable in humans. Inocculate humans with mutated virus--Immune response induced w/out symptoms or pathology.
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| Recombinant DNA Vaccination | Isolate virus and either mutate or delete virulent coding regions. Inocculate human with broken virus--Immune response evoked w/out symptoms or pathology
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| Peptide Vaccines | Given knowledge of a particular HLA marker that is assoc. w/ resistance to disease, identify viral nonamer peptides with similar characteristics to HLA binding site. Test peptides's binding for induction of T-cell response. E.g melanoma MAGE's
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| DNA vaccines | Isolate pathogen genes coding for immunogenic proteins. Inject DNA IM. Sometimes works? Why--beats me.
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| Corticosteroid Therapy mechanism | (Steroid freely crosses cell membrane), contacts steroid receptor:Hsp90 complex. Hsp90 complex displaces and Steroid:receptor enter nucleus and effect gene transcription with anti-inflammatory effects
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| Effects of Corticosteroids on Immune system | Decrease in Pro-inflammatory cytokines and activity of enzymes for prostaglandins and leukotrienes, decreased lymphocyte migration; apoptosis induced via endonucleases in Lymphoblasts and eosinophils
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| Side effects of corticosteroids | Fluid retention & weight gain, diabetes (insipidus?) bone mineral loss & thinning of the skin SO ALWAYS USE LOWEST USEFUL DOSE
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| Cytotoxic Immunosuppressive drugs | Interfere with DNA synthesis by blocking purine or thymidine synthesis, or alkylating DNA
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| TNF-α as an anti-inflammatory in autoimmune disease | Effective as seen in Rheumatoid Arthritis by decreasing pain, joint swelling, and presence of C-Reactive protein
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| Anti-MHC class II Antibody therapy in autoimmune diseases | Blocks pAPCs from presenting self antigen to CD4 Th1 cells; thus no cytotoxic effects on self. Not yet useful b/c the effects also disable CD4 Th2 cells from producing antibody stimulating cytokines.
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| Tumor causing viruses | Have been seen for various tumors. Viruses include HPV, Hep. B, EBV, Human T-Cell Leukemia virus 1 (HTLV-1) and HIV
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| Tumor rejection antigen and tumor immunity | antigens are specific for individual tumors. If person expresses appropriate MCH able to recognize antigen, tumor is rejected. If not, tumor grows and person dies.
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| How does our normal immune system handle tumors when possible? (Tumor rejection antigens) | 3 ways: MHC I molecules express specific mutated peptide antigens recognized by CD8 T cells; tumor reactivates embryonic genes' proteins expressed by MHC I & killed; Overexpression of normal self protein--seen as irregular by T cell
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| How do tumors escape immune recognition? | 3 ways: By expressing no MHC, adhesion molecules or costimulators; Endocytosing anti-tumor Ab bound to surface--no Fc receptors present outside to signal phagocytes; Secreting factors (e.g. TGF-β) that inhibit T cells
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| Tumors and loss of MHC I expression | Decreases antitumor capabilities of CD8 T cells, but decrease is partially offset by increased killing ability of NK cells
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| Tumor-specific peptide vaccines | Effective in inducing anti-tumor CD8 effector T cells sensitized specific peptides to proliferate and kill tumor cells. E.g. MAGE-1 and MAGE-3 in melanoma
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| Tumor immunity via cross presentation | Dying tumor cells slough off particles-->endocytosed by dendritic cells. Peptides from the particle presented by both MHC I and MHC II pathways to activate CD4 & CD8 T cells-->mount immune response against those peptides
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| Tumor Therapy via monoclonal antibody with toxin/radioisotope | Monoclonal Ab's specific for tumor are injected. Can present Fc receptors to NK cells, be endocytosed with toxin to kill cell, or be in vicinity and irradiate tumor cell.
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| Enhancing tumor immunogenicity by transfecting with gene for B7 or GM-CSF | Tumor cell formerly could not express B7--no immune response. B7 now allows activation of CD8 T cells; Induction of GM-CSF production by tumor cell recruits dendritic cells to present antigen to T cells--->Dead tumor
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| Graft Rejection Memory and Specificity | (Memory/1st Set Rxn)--Rejection of 1st graft from donor will lead to more rapid rejection of subsequent grafts from that donor. (Specificity/2nd Set Rxn)--Rejection of subsequent grafts are specific to donor or twin; 2nd grafts from others--1st Set Rxn
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| Rejection & Minor Histocompatibility Loci | RATE OF graft rejection is proportional to # of loci mismatches that result in AA polymorphism between donor and self proteins (in addition to rejection due to MHC mismatching allografting--acute rejection)
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| Etiology of Allograft rejection | T Cell-Mediated and thus subject to cell memory; showing both 1st set and 2nd set characteristics; Antigen presented by both Donor APC (Direct allorecognition) and by Recipient APCs (Indirect Allorecognition)
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| Direct Allorecognition | Recipient's T-Cells stimulated by DONOR APSs in lymph node--(Recognized a foreign MHC)
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| Indirect Allorecognition | Proteins from the graft are endocytosed and processed by RECIPIENT APCs
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| Testing donor compatibility with Mixed Lymphocyte Reactiona dn Cr-Release assay | (MLR) reflects if immune response (T-Cell prolif) will occur. Cr-Release assay reflects if donor T-cells will kill host cells. *Compatible donor will have low levels from each of these tests
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| Hyperacute Graft Rejection | Occurs when recipent, for whatever reason, already has circulating Ab from prior exposure to Donor MHC--Prevent by crossmatching donor blood with recipient serum (antibodies) in vitro.
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| Graft Tolerance in the Fetus--Why? | possible expantations include that placenta (trophoblast?) cells express no MCH; Or the fetal/placental secretion of Th2 incducing cytokines (which block prolif. of Th1 cells' promoting cell mediated immunity)
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| Monoclonal Ab therapy to inhibit allograft rejection | Anti-CD4 Ab given with 1st allograft can inhibit 1st set response, and confers Specific Tolerance such that subsequent allografts will not elicit an immune response--Successful in mice, but causes complications in humans
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| GVHD differences from other rejections | GVHD (only in Bone marrow transplants) involves DONOR Lymphocytes attacking HOST cells (opposite mechanism as, e.g. rejection of kidney allograft)
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| Chronic Graft Rejection (***Different from GVHD***) | Stimulation of Indirect allorecognition pathway results in Anti-Donor-HLA I alloantibodies (from host) attack blood vessels of transplanted organ; causing increasing vascular damage over time and ultimate rejection.
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| Factors excluding candidate for organ transplant | Infections (e.g. HIV, CMV, syphilis, etc.), malignancies, vascular diseases (e.g. MI), likelihood of noncompliance
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| Induction Therapy to prevent acute graft rejection (Hyperacute prevented by crossmatching) | Zenapex/Simulect (partial humanized monoclonal Ab) Relatively new--replaced toxic, single use OKT3--very effective, but expensive. Targets CD3 without allergic reaction to "box" immune system for that time
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| Maintenance Therapy (for after Induction therapy) to prevent graft rejection | Prednisone and Cyclosporin or tacrolimus (FK605), and a purine synthesis inhibitor (Cellcept or Imuran) and a host of other meds to protect from infections or side effects
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| Antirejection Therapy (when graft begins to reject) | High dose Prednisone (when discontiuned can trigger Addisonian crisis), OKT3 (single dose when steroids inneffective--causes allergic rxns), Thymoglobulin is last chance.
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| Common causes of diminished renal function post transplant | Acute/chronic rejection, acute tubular necrosis-->ischemia increases MHC expression, Cyclosporin/tacrolimus (nephrotoxic themselves), Infections
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| Factors promoting graft survival | Younger donor, low cold storage time; minimal antigen mismatches; absence of primary or coexisting diseases, early rejection episodes; low reactive Ab level in serum
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| MALT specializations promoting IgA production | Predominant Th2 cell population produce TGF-β and IL-5 promote class switch to IgA
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| Preferential migration ot mucosa by mucosa derived lymphoblasts | complementary lymphoblast/mucosal vascular endothelium (α4β7 integrin/MAdCAM-1) ensure IgA secreting cells will tend to go to mucosal and secretory sites
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| T cells and Mucosal Immunity | Esp. important against fungi and mycobacteria. Very prominent in gut & nearly all lymphocytes @ epithelium. Increased prominence of γδ/CD8 T cells @ intraepithelial compartment--regulate renewal & repair of mucosa via cytokines produced.
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| Oral Tolerance, Th2 cells mechanisms and advange | Systemic unresponsiveness to harmless antigen ingested PO--route of entry presents antigens to mostly Th2 or CD8 Treg cells-->TGF-β & IL-10 suppress cell-mediated Th1 resp. while exposing antigen to system-->future tolerance via clonal deletion/anergy
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| T Cells and IL-5 (from T & stromal cells) involved in Asthma Onset | Neither required for increased production of CFU-eo in marrow, but ARE required for accelerating eosinophil MATURATION in marrow
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| Stem Cell Factor (SCF) and asthma onset | Is responsible for increased CFU-eo during asthma onset; independent of T cell involvement--probably from marrow stromal cells
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| Cysteinyl leukotrienes and onset of asthma | responsible for initial depression in marrow CFU-eo, and not responsible for subsequent accelerated CFU-eo production. ONLY CONTRIBUTE to increased eosinophil maturation in marrow
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| IL-4 and onset of asthma | Actually suppresses CFU-eo production during onset (dampening effect on systemic reaction)
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| Genetics of Chronic asthma | Some phenotypes (A/J mice) are susceptible to fibrosis, increased CFU-eo and eosinophil production; whereas other phenotypes (BALB/c mice) develop tolerance to antigens & suppress eosinophil response to long term exposure
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| Characteristics of Chronic Asthma (5) | Pulmonary eosinophilia, Airway mucus plugging, peribronchial fibrosis, increased bone marrow CFU-eo and mature eosinophils
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