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35 Cards in this Set
- Front
- Back
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marker for mast cell activity (useful in anaphylaxis)
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tryptase
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What does HLA encode for
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HLA encodes for MHC which present antigen fragments to T cells and bind TCR.
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Which HLA code for MHCI
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HLA-A, HLA-B, HLA-C code for MHC-I
expressed on almost all nucleated cells, NOT RBCs though. |
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How is the antigen loaded on MHC I
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antigen is loaded in the RER
pairs with B-2 microglobulin, which aids its transport to the cell surface. MHCI binds TCR and CD8 |
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Which HLA code for MHC II?
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HLA-DR, DP, DQ
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How is the antigen loaded on MHC II?
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Antigen is loaded following release of invariant chain in an acidified endosome.
Structure is alpha and beta globulin chain. Binds TCR and CD4 |
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Which diseases are associated with HLA
-A3 -B27 -B8 |
-A3: hemochromatosis (increased transfer of iron to transfferin --> cirrhosis, bronze diabetes, cardiomyopathy
-B27: Psoriasis*, ankylosing spondylitis, IBD, reiter's -B8: Graves |
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DR2
Which diseases are associated with HLA: DR2 DR3 DR4 DR5 DR7 |
DR2: multiple sclerosis, hay fever, SLE, goodpastures
DR3: DM1 DR4: rheumatoid arthritis, DM1 DR5: pernicious anemia, Hashimotos DR7: steroid-responsive nephrotic syndrome |
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Two signals for helper T cell activation
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1. antigen presented on MHCII and recognized by TCR on Th cell.
2. costimulatory signal = B7 on CD28 on Th |
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Two signals for cytotoxic T cell activation
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1. Antigen from MCI binding TCR on Tc
2. IL-2 from Th1 cell binds IL-2 receptor on Tc |
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Two signals for B cell class switching
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1. IL-4,5,6 from Th2 cell
2. CD40L on Th2 binds CD40 on B cell |
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What inhibits Th2 cell?
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INF-Y
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What inhibits Th1 cell?
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IL-10
Think of IL-10 as an inflammatory response mediator. It is secreted by regulatory T cells. |
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Th1 participate in which response?
secrete what cytokines |
cell mediated response
secretes IL-2 --> CD8 secretes INF-Y --> macrophage |
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Th2 participate in which response?
secrete what cytokines |
humoral response
secretes IL-4 (IgE, IgG) IL-5 (IgA, eosinophils) |
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crosses the placenta
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IgG (monomer)
opsonizes bacteria, neutralizes bacterial toxins and viruses main Ig in 2ndary response, most abundant in blood. |
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When is IgA a monomer, dimer
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monomer in circulation
dimer when secreted (in tears, saliva, mucus, colostrum) |
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pentamer immunoglobulin
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IgM
however, is a monomer on B cell receptor |
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how do we fight helmenths
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free IgEW binds Fc receptor on eosinophil which releases major basic protein and kills worm/parasie
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What are the 2 C5 convertases
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If its by the lectin (from microbial surfaces) or classic pathway(from antigen-antibody complexes) C5 convertase = C4b,2a,3b
If its by the alternative pathway = C3bBb,C3b |
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what are the two anaphlatoxins
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C3a, C5a
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what two things prevent complement activation on self cells?
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DAF: defect --> paroxysmal nocturnal hemoglobinuria
C1 esterase: hereditary angioedema* never treat a person with ACE I (both lead to increased bradykinin --> angioedema) |
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5 main effects of complement
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1. lysis of pathogen via MAC
2. generate anaphylatoxins C3a, C5a (bind to mast cells --> histamine, bind directly to bronchioles --> bronchospasm) 3. chemotaxis via C5a attracting neutrophils 4. opsonization via C3b receptors on macrophage taking up bacteria 5. C3b increases antibody formation |
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IL-6 fxn?
IL-8 fxn TNF-alpha fxn |
IL-6: endogenous pyrogen, fever, acute phase proteins (similar to IL-1, but doesn't recruit leukocytes)
IL-8: neutrophil chemotaxis TNF-alpha: mediates septic shock, leukocyte recruitment, vascular leak |
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alpha and beta interferons
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inhibit viral protein synthesis, secreted by a wide variety of eukaryotic cells and work on neighbor cells
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Y-interferons
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increase MHCI and II expression, secreted by Th1
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common variable immunodeficiency
presentation, labs |
defect in B cell maturation --> normal number of B cells, but lower plasma cells
can be aquired in 20-30s increased risk of autoimmune disease, lymphoma, infections |
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immune deficiency that causes disseminated mycobacterial infections
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IL-12 receptor deficiency, causes decreased Th1 response and labs show decreased INF-Y
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Job's syndrome (hyper IgE)
5 characteristics in presentation labs |
Pathogenesis: Th cells fail to produce INF-Y --> inability for neutrophils to respond to chemotactic stimuli.
Presentation: coarse Facies, cold staph Abscesses, retained primary Teeth, hyper IgE, Derm problems (eczema) |
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3 causes of SCID
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1. X-linked defective IL-2 receptor: deceased T cell activation for Th1/Th2. (most common)
2. Adenosine deaminase deficiency: ADA decreades adenosine --> inosine and without it will lead to toxic concentrations of ADP/AMP which inhibit ribonucleotide reductase which converts UDP --> dUDP, ultimately making dTMP. 3. Failure to synthesize MHC II; decreased T and B cell class switching Rx: bone marrow transplant (won't reject the allograft) |
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Triad of ataxia telangiectasia
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cerebellar defects
spider angiomas (telangiectasia) IgA deficiency *caused by defect in DNA repair enzymes |
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Wiskott Aldrich syndrome
-pathogenesis -triad -labs |
X-linked progressive deletion of B and T cells
Thrombocytopenic purpura Infections Eczema *labs show increased IgA/E, but decreased IgM |
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recurrent bacterial infections, absent pus formation and delayed separation of the umbulicus
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Leukocyte adhesion deficiency
defect in LFA-1 itegrin (CD18) labs = neutrophilia (can't adhere so they are just floating in the blood, no neutrophils in wounds = no pus formation) |
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chediak higashi triad
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pyogenic infections staph, strep
partial albinism peripheral neuropathy |
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negative nitroblue tetrazolium dye reduction test are susceptible to what 3 specific infections?
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chronic granulomatous disease
lack of NADPH oxidase (can't make ROS which create h202) susceptible to S. aureus, E coli, aspergillus |
