Antibody function Flashcards
What does IgA do to prevent pathogen invasion
covers the virus cell to surface antigens, therfore its difficult for pathogen to bind to target.. secreted my mucosal cells.
What does IgG + IgM antibodies prevent
if pathogen is already in tissue they prevent it adhering to blood vessel walls, cell membrane + extracellular matrix.
toxins (good antigens) are counteracted by antitoxins. how does this mechanism work and how do yuo obtain a antitoxin
antitoxin prevent toxic action by distorting active sites
. animal is immunized with toxoid (inactivated toxin by formalin heat). Then the animals serum is used to relieve patients suffering from toxin (passive immunization)
. eg tetnus vaccine / being immunizixzed with anti venom vaccine)
how does antiserum for deathstalker scorpion work.
toxin = chlorotoxin, blocks chloride ion channels in muscles + causes paralysis. specific antibodies bind to it and doesnt allow it to block these channels
How does the antibody work indirectly
.Constant part of heavy chain (Fc fragment) recognized by complement components + (Fc receptors) on phagocytes +mast cells.
. antibody = adaptor molecule, binding to antigen on one side, + participants in innate immunity, on the other side.
. Antibodies works with complement and phagocytes
Antibody recognizes + the other 2 destroy it. ENHANCES INATE IMMUN
OPsonisation with IgG and IgM
. Phagocytes have Fc receptors for IgG. So IgG
antibodies opsonize
. IgM and IgG opsonize indirectly - activates complement.
Therefore, surface around IgM +IgG
antibodies is covered by C3b, which has an
opsonizing function.
Classical complement system stages
. C1 composed of C1q (main), C1r and C1s. It recognizes Fc fragment of IgM + IgG.
. Their heads bind the antibodies
.Binding of C1q to antibodies activates C1r, then activates C1s.
. C1s cuts the next component, C4.
. C2 is cleaved by C1s
. C2b goes while c2a binds to c4b
. makes c3 convertase (c4b2a) which splitsc3 into a + b
.c3b binds to c4b2a + makes c5 convertase.
. cleaves to c5a +c5b
. c5b binds to c6,7,8,9, and makes membrane attack complex
. this penetrates membrane of pathogens/ cell lysis
what is purpose of IgE in inflammation
. mast cells + basophils hv Fc receptos for IgE. their binding induces exocytosis of granules causing inflammation
what does Immunoglobin M do
** first to appear in dvlpmt + differeniaon of every B cell
. Has multimeric structure, so has high valency
compared to other immunoglobulins.
Allows IgM to compensate for low
affinity + bind to target antigens with
high avidity (binds multiple antigen particles).
. IgM binds to antigens with repeated epitopes, which allows agglutination.
*** its best activator of classical pathway + is confined to bloodstream
what does immunoglobin G do
** very prevalent in secondary response
. can easily crosses capillary walls
. only immunoglobin to cross placenta to protect the foetus.
. also oponizizes through Fc receptors on phagocytes
what does Immunoglobin A do.
** in saliva, tears, sweat ….
. protects the mucosal surface.
. binds to the surface of micro organisms + prevents them adhering to mucosal epithelial cells.
** beloongs to mucosa assoc lymphoid tissue (MALT)
what are the 2 types of IgA
. Secretory IgA - has 2 covalently linked IgA molecules
by additional J chain and are also
covalently linked with secretory component
. Dimeric IgA - binds to poly-Ig receptor on
basolateral membrane of epithelial cell + is
internalized by endocytosis. After transport of the
receptor-IgA complex to the luminal surface,
poly-Ig receptor is cleaved,+ releases secretory component
name 4 IgA defence mechanisms
- synthesis of secretory IgA
- Antigen clearance from lamina propria
- Cross protection against diverse pathogens ( 1 antibody against many pathogens wth similar epitopes)
- intracellular virus neutralization
What is immunoglobin D
Exists mostly in membrane-bound
(receptor) form.
. functions in B cell differentiation rather than in humoral response.
what is Immunoglobin E
. Secreted into the serum, where mast cells + basophils take it + hold it on Fc receptors.
** IgE attaches to its Fc receptors before binding antigen. (unlike IgG)
. If this adsorbed IgE binds to antigen/ hapten, this causes degranulation of the mast cell, causes inmflamm response
. IgE protects tissues from pathogens that have crossed IgA- guarded first line of defence. Useful against large parasites (helminths).
What are natural antibodies
IgM IgA IgG
aacts as first line of defence
Natural IgM protects against viral, bacterial, fungal and parasitic infections.
Has polyreactivity + high valency which facilitates binding to pathogens + enhances pathogen neutralization + agglutination.
What are natural autoantibodies
. react with damaged and senescent (non dividing) cells
promoting their clearance.
what are hypersensitivity/allergy reactions
more harm than good
three forms:
- When the immune system by mistake reacts against
a self antigen. - When the immune system reacts against a foreign
antigen which is harmless - When an initially appopriate immune response
against a foreign antigen becomes destructive
because of its excessive intensity and/or duration.
TYPE 1 IgE mediated
. Antigens + haptens
Triggering it = allergens Eg pollen, dust,
food components, drugs .
. Exposure to the allergen causes massive
mast cell degranulation and out-of-control inflammation.
anaphalaxys may develop
TYPE 2
. Cells inappropriately killed by the immune system
after being covered by antibodies.
Two ways lead to thedeath of target cells:
1) Complement activation by IgM or IgG;
2) Opsonization by IgG.
. Lead to hemolysis in Rhesus-incompatible
pregnancy +incompatible blood transfusion.
TYPE 3
Immune complex mediated hypersensitivity
. When the antigen is in excess for a long time, immune complexes circulate (when they are normally ridden from bloodstream), in kidneys, joints and skin,
. Causes chronic inflammation.
. “serum sickness” of patients who have received twice
antitoxin from same animal species.
. After 1st infusion, antibodies are produced against
the animal proteins.
. After 2nd infusion, antibodies bind their antigens, forming large quantities of immune complexes.
What is Frustrated phagocytosis
BASO WHEN PHAGOCYTES CANT ENGULF THE COMPLEX
When complexes adsorbed
on basement membranes.
Cant engulf the complex,
phagocytes exocytose their granules over it.
This damages nearby cells + membrane. causes arthritis