IMMUNOLOGY
Heavy & Light chain regions
Binds antigen but doesn't activate effector mechanisms
lo concentration in serum
bound to mast cells & basophils
initiates allergic rxn & anaphylotic shock
induces histamine release
low affinity, avidity and titer
1st encounter w/ the foreign antigen
memory cells generated
primarily IgM antibodies
2nd method of destruction
C3 binds & promotes its assembly
resembles a hollow tube, inserts itself into the membrane, H20 flows in causes the cell to bursts
Heavy chains only
Activates effector mechanisms after antigen binds, allowing for AB destruction
Bound to membrane of a beta cell
minimum levels in serum
unknown function
Lysis of antibody coated cells
Mediates opsonization
regulates features of the inflammatory & immune response
"largest"
Doesn't cross placenta
predominate Ig during fetal development
Hi avidity due to 10 binding sites
High affinity, avidity and titer
2nd encounter w/foreign antigen
memory cells engaged
Primarily IgG antibodies made
Cells are cleared in the liver/spleen not in the intravascular space
Caused by IgG red cell anitbodies
RBC consumption by phagocytes
Most abundant in serum
"lightest"
small enough to cross the placenta
Conformational change of IgM after binding the antigen, this initiates complement cascade
And 2 IgG's bind in clusters on the same target of the complement cascade
dominant in secretions
deficiency in transfusion rxns
monomer in serum
undetectable w/DAT
neutralizes foreign invaders & only picks up IgG
The target is covered w/ complement components and is marked for destruction
C3 is converted to C3b and is recognized by phagocytes
C3b can be degraded into C3dg, this will become unrecognizable by phagocytes & is bypassed
Lysis occurs while still w/vasculature
Signs & symptoms of AHTR
Caused by IgM red cell antibodies
Cell destruction by MAC