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HUMORAL-MEDIATED IMMUNITY - Coggle Diagram
HUMORAL-MEDIATED IMMUNITY
EFFECTOR FUNCTION OF ABS
AB IN THE FOETUS
Abs are primarily IgG - acquired by transfer of maternal IgG across the placenta
Some Ab are made by foetus in infection occurs (congenital syphilis)
Newborn infants can make IgG - for certain antigens
Application: Vaccine against HBV contains Hepatitis B surface Ag is effective for newborns
Maternal IgG declines after birth & protection from maternal IgG is lost by 3-6 month
AB PROTECTION AGAINST TOXINS
Toxins consists of separate domains for exerting toxicity binding to a specific cell surface receptor which they enter the cells
Bacteria causes diseases by secreting toxins
NEUTRALIZATION - Abs bind to toxin's receptor to prevent cell entry & protect cell fro, attack
HIGH AFFINITY ABS
Toxins are active at nano molar
Abs is able to diffuse into the tissue & bind to toxin rapidly with affinity
The affinity of the Abs is depend on the site of infection
EFFECTOR FUNCTION OF FC RECEPTOR OF AB
Function of Fc:
clearance of antigen-antibody complexes (immune complex, IC) from circulation
Fc receptor expressed on various phagocytic cells
If IC is not removed from circulation > deposit in basement membranes of small blood vessels
Associated with autoimmune disease
(SLE) - masive deposition of IC on podocytes - kidney failure
FC RECEPTORS ACTIVATE NK CELLS
NK cells can recognise & destroy Ab coated target cells by ADCC. This is triggered when Ab bound to the surface of a cell interact with Fc receptors on the NK cells. Virally infected cells also get the signal of the presence of intracellular infection (viral envelope protein recognised by Ab)
ABS DEFICIENCIES RELATED DISEASES
HYPER IgM SYNDROME
Defects specific to activation & differentiation of B cells > impair class switching while leaving cell mediated immunity largely intact
Hyper IgM syndrome - CD40 ligand deficiency
Patients are susceptible to infection with extractllular pathogens
PRIMARY IMMUNODIFICIENCY
COMMON VARIABLE IMMUNODIFICIENCY
Most common form of primary immunodificiency
A clinically & genetically heterogenous group of disorders that typically go UNDIAGNOSED until late childhood or adulthood
Immune deficiency relatively mild
Patients present with defect in Ig produced that limited to one or more isotopes
IgA DEFICIENCY
Most common - sporadic & familial forms
Autosomal recessive & dominant inheritance
Majority are asymptomatic - IgA deficient patient with recurrent infection - assoc with defect in one IgG subclasses
CLASSICAL COMPLEMENT IMPORTANT EFFECTOR TO AB RESPONSE
Coat pathogen surfaces / Ag with Ab to form
antibody-antigen complexes
The complex is covalently attached C3b (complement fragment) - acts as opsonin -
promote uptake & removal by phagocytes
The terminal complement components can form
membrane-attack complex
> cytolysis