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81 Cards in this Set
- Front
- Back
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Origin of the thymus
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3rd branchial pouch
mesenchymal |
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CD8 cells bind to MHC class:
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I (8 x 1 = 4 x 2)
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CD4 cells bind to MHC class:
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II (8 x 1 = 4 x 2)
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CD4 cells become Th2 cells in the presence of:
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IL-4
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CD4 cells become Th1 cells in the presence of:
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IL-12
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Th1 cells make the following cytokines:
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IL-2 and INF-gamma to activate mphage and CD8 cells
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Th2 cells make the following cytokines:
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IL-2, IL-4 and IL-5 and help B cells make antibodies
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MHC-I and MHC-II molecules are expressed on these cells:
What genes are they encoded on? |
MHC - 1 = almost all nucleated cells
MHC - II = APCs only Encoded on the HLA genes of chromo 6 |
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What is the TCR complex composed of and what cells is it on?
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TCR
CD-3 --> for cell signaling delta chain It is on CD4 and CD8 cells |
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For CD4 cells, what are the molecules on the APC that bind to what molecules on the T cell?
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MHC II on APC - TCR on T cell (signal 1)
B7 - CD 28 (signal 2, costimulation) CD 40 - CD 40L (which tells APC to make more B7) |
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For CD8 cells, what are the 2 signals needed for activation?
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signal 1: MHC-I bound to TCR
signal 2: IL-2 from the CD4 cells |
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What are the characteristics of the Fab fragment of an antibody?
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amino terminal
contains the hypervariable regions on the light and heavy chains responsible for antigen recognition |
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What are the characteristics of the Fc fragment of an antibody?
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Constant (no variability, all heavy chains)
Carboxy terminal Complement binding (to IgM and IgG) Has carbohydrate side chains |
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The mature B lymphocytes first express these types of Ig's (before isotype switching)
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IgM and IgD
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IgG
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secondary response.
Most abundant Fixes complement the only one that crosses the placenta opsonizes bacteria, toxins, viruses |
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IgA
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Prevents attachment to mucous membranes
Does not fix complement Monomer or dimer Picks up secretory component from endothelial cells |
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IgM
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Primary antigen response
Fixes complement Monomer or pentamer |
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IgD
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unknown fxn
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IgE
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Mediates type I hypersensitivity reaction
--> release of mediators from mast cells and basophils Mediates immunity to worms Lowest concentration in serum |
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IL-1
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Made by: mphages
Stimulates: T cells, B cells, mphage, epithelial cells Causes: fever |
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IL-2
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Made by: Th1 and Th2 cells
Stimulates: CD4 and CD8 cells Causes: growth |
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IL-3
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Made by: activated T cells
Stimulates: Bone marrow stem cells Causes: growth and differentiation (like GM-CSF) |
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IL-4
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Made by: Th2 cells
Stimulates: B cells, T cells Causes: Growth, enchances class switching to IgE. Increases differentiation to Th2 cells |
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IL-5
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Made by: Th2 cells
Stimulates: B cells, eosinophils Causes: class switching to IgA. Increase in eosinophils |
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IL-6
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Made by: Th1 and Th2 cells and mphages
Causes: production of acute phase reactants and Ig |
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IL-8
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Causes: neutrophil chemotaxis
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IL-10
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Made by: Th2 cells
Stimulates: Th2 and Th1 cells Causes: stimulates Th2 cells, inhibits Th1 cells |
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IL-12
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Made by: B cells, mphages
Stimulates: NK and Th1 Causes: activation, increase in Th1 differentiation |
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gamma-interferon
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Made by: Th1 cells
Stimulates: Macrophages Causes: increase in MHC I and II expression and antigen presentation |
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TNF-alpha
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Made by: mphages
Stimulates: Th1 and Th2 and B cells, neutrophils Causes: Increase in IL-2 production, increase in B cell proliferation, neutrophil activation, dendritic cell migration to lymph nodes |
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TGF-beta
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Made by: CD4 and others
Causes: inhibition of T cell activation |
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Complement defends against this type of bacteria:
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gram negative
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The classic pathway is activated by:
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IgG or IgM
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The lectin and alternative pathways are activated by:
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microbial surface proteins
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The classic and alternative pathways converge at this complement component:
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C3 in each --> C5 --> C5b, 6, 7 --> membrane attack complex (C5b, 6, 7, 8, 9) --> lysis
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Interferons work by:
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inducing the cellular production of proteins that inhibit viral protein synthesis by degrading viral mRNA
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Deficiency in C1 esterase inhibitor causes:
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hereditary angioedema from overactive complement (classic pathway)
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Deficiency of C3 causes:
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severe recurrent pyogenic sinus and respiratory infections
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Deficiency of C6-C8 causes:
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Neisseria bacteremia
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Deficiency of decay-accelerating factor (DAF) causes:
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paroxysmal nocturnal hemoglobinuria (PNH)
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Type I hypersensitivity
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IgE on presensitized mast cells and basophils --> vasoactive amine release
Due to preformed antibody mediators: Th2, mast, IgE, eosinophils examples: Allergic rhinitis, bronchil asthma, anaphylaxis |
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Type II hypersensitivity
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Antibody mediated - IgM and IgG attacks cell --> complement lysis or phagocytosis.
Examples: Graves, Hashimotos, Pernicious anemia, pemphigus, transfusion rxns, rheumatic fever, farmers lung |
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Type III hypersensitivity
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Immune complex mediated - IgG and IgM
Complement is activated (classic), neutrophils are activated. Complexes deposited in skin, kidney, joints Causes local vasculitis Examples: serum sickness, rheumatoid arthritis, glomerulonephritis, sxs of malaria and SLE |
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Type IV hypersensitivity
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Delayed, T cell mediated
Takes 2-3 days to occur Lymphocytes activate mphage --> giant cells Examples: Contact dermatitis (poison ivy), temporal arteritis, transplant rejection, celiac disease, sxs of leprosy and TB (PPD) |
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Type V hypersensitivity
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Like type II but in Britain where the Abs bind to specific cell receptors
Ex/ Myasthenia gravis and graves disease |
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Name that hypersensitivity reaction:
1. Guillain-barre 2. ITP 3. Bullous pemphigoid 4. Lupus 5. Post-strep glomerulonephritis 6. Arthus reaction 7. Hypersensitivity pneumonitis |
1. Type IV
2. Type II 3. Type II 4. Type III 5. Type III 6. Type III 7. Type III |
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Bruton's agammaglobulinemia
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X linked recessive
defect in tyrosine kinase gene Pre-B cells can't mature Low levels of all immunoglobulins Sxs: bacterial infections after 6 mo Path: no tonsils, apparently nl thymus |
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DiGeorge syndrome
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22q11 deletion
Thymic aplasia due to failed development of the 3rd and 4th branchial pouches Sxs: hypocalcemia, tetany, T cell absence, recurrent viral and fungal infections Path: heart defects, great vessel defects |
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SCID
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Caused by: mutant IL-2 receptor, adenosine deaminase deficiency, failure to synthesize MHC-II proteins.
Sxs: failure to thrive, opportunistic infections |
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IL-12 receptor deficiency
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Presents with disseminated mycobacterial infections
(it is supposed to stimulate Th1 differentiation and NK cells) |
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hyper-IgM syndrome
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Defect in CD40 ligand on CD4 cells
Inability to class switch Sxs: elevated IgM, very low everything else, severe pyogenic infections |
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Wiskott-Aldrich syndrome
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X linked
No IgM response to bacterial capsules Primary defect unknown Sxs: elevated IgA, low IgM, nl IgE. Recurrent pyogenic infections, thrombocytopenic purpura, eczema, increase in malignancy and lymphoma |
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Job's syndrome
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Failure of gamma-interferon production by helper T cells
No neutrophil chemotaxis Sxs: noninflamed staphylococcal abscesses, eczema, coarse facies, retained primary teeth, high levels of IgE |
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Leukocyte adhesion deficiency syndrome
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Defect in LFA-1 adhesion proteins on phagocytes
Sxs: severe pyogenic and fungal infections, delayed umbilical separation |
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Chediak-Higashi disease
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Autosomal recessive
Defect in MT fxn and lysosomal emptying of phagocytic cells (lysosomes and phagosomes can't fuse) Sxs: recurrent staph and strep infections, partial albinism, peripheral neuropathy |
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Chronic granulomatous disease
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Lack of NADPH oxidase activity
Decrease in neutrophil fxn Sxs: opporutinistic infections (S. aureus, E. coli, Apergillus) Dx: negative nitroblue tetrazolium dye reduction test |
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Chronic mucocutaneous candidiasis
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T cell dysfxn against Candida
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Selective immunoglobulin deficiency
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Most commonly an IgA deficiency
Sxs: chronic sinus and lung infections, milk allergies, diarrhea |
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Ataxia-telantiectasia
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Defect in DNA repair enzymes
IgA deficiency Sxs: cerebellar problems, spider angiomas |
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Common variable immunodeficiency
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Normal levels of B cells but decrease in plasma cells and Ig
Can be acquired in 20-30s |
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Antinuclear antibodies
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SLE, nonspecific
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Anti-dsDNA
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SLE, specific
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Anti-smith
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SLE, specific
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antihistone
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Drug-induced lupus
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anti-IgG
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= rheumatoid factor
RA |
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antineutrophil
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= p-ANCA, c-ANCA
vasculitis |
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anticentromere
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scleroderma (CREST)
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anti-Scl 70
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scleroderma (diffuse)
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antimitochondiral
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primary biliary cirrhosis
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antigliadin
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celiac disease
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anti-basement membrade
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goodpastures
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anti-epithelial cell
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pemphigus vulgaris
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anti-microsomal
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hashimoto's thyroiditis
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anti-Jo1
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polymyositis, dermatomyositis
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HLA-B27
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Psoriasis
ankylosing spondylitis inflammatory bowel disease reiter's syndrome |
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HLA-B8
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Graves
celiac sprue |
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HLA-DR2
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MS
hay fever SLE goodpastures |
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HLA-DR3
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DM type I
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HLA-DR4
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RA
DM type I |
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HLA-DR5
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pernicious anemia
hashimotos |
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HLA-DR7
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steroid-responsive nephrotic syndrome
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