Humoral Effector Mechanisms (Intervention) Flashcards
1. antibody mediate opsonization (IgG) 2. NK cytotoxicity (IgG) 3. Mast Cell Reactions (IgE) 4. Classical Complement Activation (IgG&M) 5. Mucosal/ Neonatal Immunity (IgA; G)
Fab region
the region of immunoglobulins that binds antigens
Etymology: scientists studying immunoglobulins digested them resulting in fragments. based on these studies they named different parts of proteins F- fragment ab- antigen binding c- constant
Fc
the region of immunoglobulins that activates effector functions
Etymology:
scientists studying immunoglobulins digested them resulting in fragments. based on these studies they named different parts of proteins
F- fragment
c- constant
after protein digests, immunoglobulins form different fragments
heavy-chain isotype switching
B-cells respond to antigen stimulation by expressing the Heavy chain (G, M, A, E) that binds antigen most effectively
affinity maturation
a process called somatic hypermutation produces slight alterations in the Fab region that produces epitopes that are better at binding anitgens
prac- reason for multiple rounds of immunization
IgM effector function
critical in primary immune resonse, it activates the classic pathway of the complement system
IgA effector functions
mucosal immunity: secretion of IgA into lumens of gastrointestinal and respiroatyr tracts, neutralization of microbes and toxins
IgE
defense against helminths and mast cell degranulation
IgG
important in secondary immune response
- activation of the classic complement pathway
- neutralization
- opsonization
- cellular cytotoxicity (direction of NK cells)
- neonatal immunity
- feedback inhibition of B-cell activation
FcRn
etymology: Fragment Constant Receptor, neonatal isoform
f(x): to spare IgG from lysosomal degradation
Fc gamma RI
f(x): promotes phagocytosis of opsonized bacteria
wh cells: expressed on phagocytes and neutrophils
wh: a receptor expressed on phagocytic cells that promotes secretion of reactive oxygen species that digest polysaccharide rich capsules and phagocytosis of particles
polysaccharide rich capsules
protect bacteria from direct phagocytosis unless reactive oxygen species secretion is stimulated by neutrophils or phagocytes
Fc gamma RIIB
f(x): important in limiting B cell response/ inflammation
wh cells: B cells, DCs, mast cells (inflammatory cells)
wh: a receptor expressed on inflammation cells that binds the Fc region of agglutinated antibodies and triggers limitation of antibody response
Fc gamma RIII
f(x): IgG directs NK cells during antibody mediated cytotoxicity
wh cells: natural killer (NK) cells
wh: antibodies coat virally infected cells and tumors. The Fc gamma receptors on NK cells directs them to kill these pathogens through degranulation
ADCC
antibody dependent cellular cytotoxicity, IgG binding to
Fc epsilon RI
f(x): IgE direct inflammatory cells to degranulate during helminthic infection/ inflammation
wh cells: mast cells, basophils, eosinophils,
wh: a receptor expressed on inflammatory cells that works with IL-5 from helper T cells to promote inflammation
complement system in innate immunity (2)
- lectin-mannose pathway: mannose binding lectin binds to pathogens
- alternative pathway: C3b particles bind to polysaccharide residues on pathogens
- both these pathways skip C1, but the lectin pathway and classical pathway share many similarities
complement system in adaptive immunity (1)
- classical pathway- IgG directed binding of C1 to pathogens activates C3 formation of a C3 convertase and subsequent effector functions of C3a and b
C3 convertase
an enzyme that cleaves C3 complement protein into C3a and C3b componenets
classical and lectin: C4b2a
alternative pathway: C3b and bb
C5 convertase
an enzyme that cleaves complement C5 into C5a and C5b (membrane attack)
classical and lectin pathways: C4b,2a,C3b
alternative pathway: C3b,Bb,C3b,C5
Membrane Attack Complex
C6, C7, C8, C9, starring C5b
formation of complements on the membrane of pathogens causes lysis
CRI
f(x): complement mediate phagocytosis
wh cells: a receptor expressed on phagocytes
wh: a receptor expressed on phagocytes that functions as an opsonin
CR2
f(x): complement mediated activation of the innate immune system
wh cells: expressed on B lymphocytes
wh: B cells bind to C3d, a complement protein coating microbes, and the receptor signaling promotes activation. This is especially potent in germinal centers
C3d
a break down product of C3 complement that coats microbes and causes B lymphocyte activation
systemic lupus erythematosus
a defciency of C2 and C4, early proteins in the classic and lectin pathways of complement activation
DAF
decay accelerating factor, a protein that limits complement activation by disrupting binding of Bb and C3b
MCP
Membrane Cofactor Protein, serves as a cofactor for “factor 1” in the reaction that degrades C3b formation
Factor 1
a protein that degrades C3b into an inactive form
C1 INH
inhibits the classical complement in its early stages
hereditary angioneurotic edema
Deficiency of C1 INH causes excessive C1 activation and leakage of fluid into the laryxn and other tissues
paroxysmal nocturnal hemoglobinuria
lysis of erythrocytes due to defective cell surface proteins that normally bind DAF, a factor that limits complement activation
TGF-beta
a cytokine that promotes isotype switching to IgA in mucosa-associated lymphoid tissues
poly Ig receptors
special receptors expressed in mucosal epithelia that allow translocation into lumenal compartments
