Hummoral immunity (bowden) Flashcards
Humoral immunity
Branch of adaptive immunity mediated by antibodies produced by B cells (Plasma cells).
Humoral immunity is the principal defense against EXTRACELLULAR pathogens
where are antibodies produced and what produces them?
lymhoid tissues/organs
Plasma cells (activated b cells)
where is the effector function of the antibody?
Fc region
what triggers Ab function?
Ag binding to Fab (V) region of the antibody
Hyper IgM syndrome
pt is deficient in antibody responses to T-dependent Ags but can make IgM to antigens that are t-independent
usually show no germinal centers in their lymph node
cannot undergo class switching and cannot make memory B lymphocytes for long-term immunity
might have to do with defect in CD40 ligand expression on T cells so can’t switch to make IgG, IgE or IgA
prone to infections (such as PCP (pneumocytsis jiroveci pneumonia)
Humoral immune response
Neutralization
Opsonization/waste management
Complement activation
Neutralization
Ab neutralize the infectivity and potential effects of infection
only requires binding to antigen and any class works
prevents microbes from gaining enter into cells
the higher the affinity the antibody for the Ag epitope the better
used alot in vaccinations
Opsonization and phagocytosis
Fc receptors on immune cell populations promote phagocytosis
opsonization is binding of Ab to microbe
binding of opsonized microbes to phagocyte Fc receptors
Fc receptors signals activate phagocytosis of microbe
killing of microbes
ADCC
antibody-dependent cell mediated cytoxicity
can be mediated by NK cells, macrophages, eosinophils, etc.
ADCC: anti-viral state
(NK cells)20 minutes since you saved your work.
NK cells express CD16 which binds to IgG that has bound to an antigen on the surface on an infected cel
this binding of CD16 with IgG (antibody) promotes killing of anti-body coated cell
IgE mediated reactions
IgE binds to Fc receptors (CD23) present on mast cells
Ag binding causes degranulation of cell
usually for killing parasites (helminth)
Activation of the complement system
in the classical pathway
IgM or IgG
Blood group antigens
sugar groups found on bacteria in the gut
toxoids
proteins that need t help for b cell activation
why is IgG better than IgM and found in 30-50 x higher concentration in our bodies?
IgM can only promote phagocytosis of bacteria by activating the C’ system
IgG can stimulate phagocytosis by binding its Fc region to Fc receptor on phagocytes AND activates the complement system
What else is CD40 expressed on?
Macrophages and dendritic cells
lack of CD40 signaling in Hyper IgM immunodeficiency leads to impaired handling of opportunist pathogens
also expressed on platelets and endothelium and epithelium cells during inflammation
X-linked HyperIgM
CD40L deficiency severely impaired production of IgG and IgA no response to protein Ags T-independent antigen response only B memory cells absent or very reduced
what does treatment with IvIg do for pt’s with autoimmune/inflammatory diseases?
engages the inhibitory FcR on B cells and possibly dendritic cells and suppresses the immune responses
waste management
antigen/antibody immune complexes form
activation of complement leads to deposition of many C3b on the immune complex
Complement receptor (CR1) on RBC’s binds the IC
In the spleen and liver, phagocytic cells remove the immune complexes from the RBC surface
Chronic infection can lead to ….
immune complex disease
persistent immune response to antigen can lead to formation of immune complexes
immune complexes themselves may become immunogenic (RA factor)
what does positive rheumatoid factor mean?
the pt is making anti-IgG IgM
so making their own IgM against their own IgG
cryoglobulins
IC’s and proteins may precipitate at s in the kidneys, small blood vessels and other organs
associated with hep C
Polyclonal B cell response
polyclonal responses of B cells means each B cells is secreting monoclonal Abs specific to a different part of the virus
confers greater likelihood of clearance of Ag
what happens when cryoglobulin complexes deposit in the wall of blood vessels?
they active C’
release of C3a and C5a are chemotactic and recruit leukocytes (macrophages and neutrophils)
neutrophils and macrophages release enzymes causing damage to endothelial cells of basement membrane
Treatment for cryoglobulenemia using CD20 does what?
this is an antibody that targets CD20 which is on B cells
targets B cells for death
it is risky b/c it is taking out the entire B cell population
