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Immuno Lec 6

IgG Highest concentration in serum. In tissue and blood longest half life. Important for passive immunization. Crosses placenta Activates Complement
IgM In Blood. monomer in B cell, pentamer in serum. Most important compliment activator. Blood borne infections. half life - 5 days.
IgA monomer in serum dimer in secretions, mucosal surfaces. J chain is in dimeric, secreted by B cell
Transcytosis of IgA across epithelium IgA binds poly Ig receptor, endocytosis of both, goes to lumen, now IgA and poly Ig receptor are cleaved enzymatically. Secretory IgA has part of the poly Ig receptor on it.
IgD Marker for mature B cell very low conc in serum
IgE lowest serum conc, shortest half life. bind to mast cells via its FC region located below epithelial surfaces, respi tract, and GI
Effector Functions of B cells carried out as a consequence of Ab/Ag binding. most mediated through Fc region. Neturalization, opsonization, ADCC, mast cell degranulation, and complement.
Neutralization IgG and IgA. Ab binds Ag, neutralizes function. Ag can no longer bind receptor. prevents toxin action, virus entry, and bacterial adhesion. Basis of Passive immunization
Active Immunization induction of an immune response by injection of an Ag. requires several weeks to months. long lasting immunity. have lag phase. activate specific T and B cells and memory.
Passive Immunization Transfer of immunity by injection of Ab. Neutralization. give when immediate risk of exposure.
Opsonization Ab mediated Phagocytosis. Carried out by macrophages and neutrophils. Major mechanism for destruction of encapsulated bacteria. Main isotype is IgG.
Mechanism of Opsonization Abs bind to target pathogen, once they bind, conformational change occurs in Fc region. Now recognizable by Mac and neutrophils.
ADCC Antigen Dependent Cell Mediated Cytotoxicity. By eosinophils and NK cells. Destruction of antibody coated cells.
NK cells- ADCC Self cell that is infected, may be cancerous. MHC1 on surface. Ab recognizes MHC1. NK binds FCy receptor, releases toxic granules.
Eosinophil - ADCC Eosinophil - receptor for IgE on surface. IgE - parasitic infections. Too big for macs/B cells. IgE binds parasite, change FC region, eosinophils bind to FC receptor now. release toxic mediates, induce inflammatory response.
Mast cell degranulation Mast Cells, coated with IgE by FC region. Many. It is preloaded, waiting. If binds parasitic infection, crosslinking occurs and degranulation occurs of histamine and serotonin. Increase Vasc Permeability, blood flow.
Complement System Three pathways. classical, alternate, lectin. consequences are membrane damage and lysis of pathogen or release of mediators for opsonization and inflammation.
Classical Complement Pathway Ag/Ab binds to bacteria. C1q needs to bind to two FC regions of IgM or IgG. q->r->s, C1s cleaves C4 and C2. a= active, b = binding.
Classical Complement Cascade Ag+Ab+C1s = AgAbC1s complex. C1s cleaves C4 and C2. C4b+C2b = C3 convertase. Cleaves C3, C3b+c4b+c2b = C4b2b3b, C5 convertase. cleaves C5, C5b= initates membrane attack complex.
What initiates membrane attack complex? C5b
What do all the a sections do? recruit inflammatory cells
Role of C3b Can activate opsonization or can join to become c5 convertase.
Formation of Membrane Attack Complex C5 into lipid bilayer, t hen c6, c7, c8, multiple copies of C9 make up the pore, then influx of fluids and molecules.
Alternate Pathway Innate. Ab surface is enough.
Alternate Pathway Activation + Cascade C3(labile). Small amts cleaved. C3b in serum.c3b+microbe = C3b complex. C3b complexes with factor B, factor D cuts B. now C3bBb which is c3 convertase. Stabilized by properitin. now c3bBbP3b , C5 convertase.
Lectin Pathway Innate. acts as opsonin. acute phase proteins produced in response to IL-6.
Lectin Pathway Activation. MBL(mannin binding leptin)=acute phase protein. MBL + MASP + CHO complex. Cleaves C4 and C2. Now you have C4b2b(C3 convertase). Add C3b, and you have c5 convertase. then follows classical pathway.
Cell surface proteins that regulate complement activity Bind c3b or Bind C8. c8 = mac inhibitory factor.
Serum proteins that regulate complement activity c1 inhibitor(prevent spontaneous activation) Factor H and I - bind c3b(enzymatic degradation) Properdin - required for alternate pathway, stabilizes C3bBb.
Complement Proteins Also opsonins C3b and C4b
Complement Proteins also anaphylatoxins c3a, c4a, c5a
Complement Proteins also chemotaxins c3a, c5a
Inherited immunodeficiency specific genetic defect
acquired immunodeficiency secondary to an underlying disordder. malnutrition, aging, viral infection. etc.
X-linked agammaglobulinemia - Bruton's no circulating B cells. BTK defect , B cells halted at Pre-B cell. increase susceptibility to extracellular encapsulated organisms. replacement therapy of gamma globulin. passively immunize them.
Antibody levels in infants at 6 months, you have low IgG because maternal transferred IgG goes away. normal IgM and IgA. more pronounced in prematures. respiratory tract infections.
Selective IgA deficiency Low IgA. other classes normal/elevated. increased allergies, autoimmunity
X-linked hyper-IgM elevated IgM. only trace levels of the rest. Tcell defect, no CD40L. no class switching.
Created by: nady