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Antibody function Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

What does IgA do to prevent pathogen invasion

A

covers the virus cell to surface antigens, therfore its difficult for pathogen to bind to target.. secreted my mucosal cells.

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2
Q

What does IgG + IgM antibodies prevent

A

if pathogen is already in tissue they prevent it adhering to blood vessel walls, cell membrane + extracellular matrix.

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3
Q

toxins (good antigens) are counteracted by antitoxins. how does this mechanism work and how do yuo obtain a antitoxin

A

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)

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4
Q

how does antiserum for deathstalker scorpion work.

A

toxin = chlorotoxin, blocks chloride ion channels in muscles + causes paralysis. specific antibodies bind to it and doesnt allow it to block these channels

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5
Q

How does the antibody work indirectly

A

.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

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6
Q

OPsonisation with IgG and IgM

A

. 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.

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7
Q

Classical complement system stages

A

. 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

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8
Q

what is purpose of IgE in inflammation

A

. mast cells + basophils hv Fc receptos for IgE. their binding induces exocytosis of granules causing inflammation

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9
Q

what does Immunoglobin M do

A

** 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

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10
Q

what does immunoglobin G do

A

** 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

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11
Q

what does Immunoglobin A do.

A

** 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)

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12
Q

what are the 2 types of IgA

A

. 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

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13
Q

name 4 IgA defence mechanisms

A
  1. synthesis of secretory IgA
  2. Antigen clearance from lamina propria
  3. Cross protection against diverse pathogens ( 1 antibody against many pathogens wth similar epitopes)
  4. intracellular virus neutralization
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14
Q

What is immunoglobin D

A

Exists mostly in membrane-bound
(receptor) form.
. functions in B cell differentiation rather than in humoral response.

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15
Q

what is Immunoglobin E

A

. 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).

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16
Q

What are natural antibodies

A

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.

17
Q

What are natural autoantibodies

A

. react with damaged and senescent (non dividing) cells
promoting their clearance.

18
Q

what are hypersensitivity/allergy reactions

A

more harm than good
three forms:

  1. When the immune system by mistake reacts against
    a self antigen.
  2. When the immune system reacts against a foreign
    antigen which is harmless
  3. When an initially appopriate immune response
    against a foreign antigen becomes destructive
    because of its excessive intensity and/or duration.
19
Q

TYPE 1 IgE mediated

A

. 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

20
Q

TYPE 2

A

. 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.

21
Q

TYPE 3

A

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.

22
Q

What is Frustrated phagocytosis

BASO WHEN PHAGOCYTES CANT ENGULF THE COMPLEX

A

When complexes adsorbed
on basement membranes.

Cant engulf the complex,
phagocytes exocytose their granules over it.

This damages nearby cells + membrane. causes arthritis

Biology (36 decks)

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