Humoral Immunity (Bowden) Flashcards
Humoral Immunity
bracnh of adaptive mediated by Ab produced by plasma cells. principal defense against extracellular pathogens
Where are the Abs produced by plasma cells and where are they functional
produced in lymphoid tissues and organs. function is at distant sites
What mediates the effecter functions of Abs
The Fc region of isotypes
What triggers function of Ab
binding of Ab to Fab (Variable) regions on isotypes
3 general schematics of Ab function
Neutralization- prevents bacterial adherence
Opsonization- promotes phagocytosis
Complement activation- lyses some bacteria
Which classes of Ab can do neutralization
any of them. only requires binding to Ag- higher affinity the better.
Which mechanism do vaccination Ab work
neutralization
What regions of Ab promote phagocytosis and deliver the signals
Fc receptors
What cells are main responders to viruses
NK
Describe the method of NK binding. or Ab dependent cell cytotoxicity ADCC
NK bind Ab coated cell by Fc R and destroy cells
IgE mediated Rxns
IgE binds Fc R on mast cells and eosinphils.
When Ag binds- degranulation of cell occurs
What is FcRn
Fc neonatal R for transporting IgG across placenta
Why is IgG more important than IgM against bacterial infection
IgG has higher affinity and not only does it activate C’ cascade but it also can bind Fc on phagocytes
how many types of Hyper- IgM immunodeficiency exist
5 all are genetic defects inability to switch class form IgM
X linked Hyper IgM immunodeficiency HIGM has what defect
CD40L expression.
sequelae of HIGM
neutropenia, failure to thrive, thrombocytopenia and anemia
What will the assay testing cells binding to CD40 in patients with HIGM look like
much much fewer cells bind
What will the assay testing cells binding anti-CD25 look like in patients with HIGM
normal because still binding IL2
Describe HIGM combined immunodeficiency
CD40 also on macrophages and monocytes and DCs and platelets and epithelium- impaired handling of opportunist pathogens- less efficient killin
What Ag response is okay in xlinked HIGM patients
Tindependent because doesn’t rely on CD40
Why are there Ab to blood group Ag but not to tetanus in patients with HIGM
cross reactive sugars of A and B don’t need Tcell help. so T independent Ag reaction
Toxin in tetanus needs T help
Tx for HIGM, mechanism?
intravenous Ig (IVIG) engages inhibitory FcR on B cells and possibly dendritic cells- suppresses immune system
Cyroglobinuria
precipitation of ICs at below 37 Celsius
Chronic infection can lead to Immune complex disease. Immune complexes may become immunogenic themselves.
What is rheumatoid factor + indicative of
patient making IgM to their own IgG
Where are ICs usually accumulating in body
glomerulus of kidney- too large to filter
Polyclonal B cell Response
by monoclonal Abs- extended Ag stimulation can lead to autoimmunity
Short term effects of a hepatitis infection
cryoglobinuria and vasculitis
more chronic effects of Hep C infection
immune mediated disorders
What can occur in non-treated Hep C infection
B cell malignancies
Hepatocellular carcinomas
Thyroid cancer
What can IC promote when deposited in wlal of blood vessels
activate C’ releasing C3a and C5a that will recruit leukocytes to area–>vasculitis
Why would a monoclonal Ab against CD20 work for patients with cryoglobinuria
CD20 on B cells- anti Ab will target for B cell death
