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Immunology > Antibody Effector Function (Exam IV) > Flashcards

Antibody Effector Function (Exam IV) Flashcards

1
Q

FcGammaRIIB1is expressed by

A

Naive B Cells, and prevents B cells for being involved in secondary responeses when there is a preexisting antibody response against the pathogen

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2
Q

Naive B cell binds pathogen

IgM + FcyRIIB1

A

Naive B cell is activated and becomes an antibody producting plasma cell

Production of low affinity IgM antibodies

Primary response

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3
Q

Naive B cell binds pathogen coated with specific anibody

A

A negative signal is giveb to the Naive B cell to prevent the activation

No production of low affinity IgM antibodies

Secondary reponse

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4
Q

Memory B cell binds pathogen

A

Memory B cell is activated and becomes an antibody-producing plasma cell

Production of high affinity IgG

Secondary response

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5
Q

First pregnancy of RhD- mother carrying a RhD+ fetus

A
  • primary immune response, IgM plus low amounts of low affinity IgG
  • Minor destruction of fetal erythrocytes by anti-RhD IgG

healthy newborn baby

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6
Q

Second and subsequent pregnancies of RhD- mother carrying a RhD+ fetus

A
  • secondary immune response, abundant, high affinity IgG transcytosed to fetal circulation
  • massive destruction of fetal erythrocytes triggered by anti RhD IgG

Anemic newborn babies

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7
Q

First and subsequent pregnancies of RhD- mother carrying a RhD+ fetus and infused with anti-Rh IgG

A
  • Primary immune response to RhD is inhibited by the prescence of RhD specific IgG

healthy newborn babies

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8
Q

RhoGam

A

Anti RhD+ response to people that are RhD-

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9
Q

IgM

A
  • first antibody to be produced in an immune response
  • Produced in pentameric form, binds pathogens strongly and activates complement through the classical pathway
  • Due to its large size, it is limited in its ability to leave the bloodstream and penetrate infected tissues

High aviditiy (10 binding sites)

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10
Q

Somatic hypermutation, affinity maturation and isotype switching lead to

A

the production of high affinity IgG and monomeric IgA

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11
Q

Smaller size of high affinity IgG and IgA allows

A

these antibodies to be able to exit the bloodstream and enter the sites of infection

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12
Q

IgG is actively transported across

A

vessel endothelium by specific receptors

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13
Q

FcRN

A

transport IgG from the bloodstream to the extracellular spaces

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14
Q

FcRn process

A
  1. Fluid phase endocytosis of IgG from the blood by endothelial cells of the blood vessels
  2. the acidic pH of the endocytic vesicle causes association of IgG with FcRn, protecting it from proteolysis
  3. When reaching the basolateral face of the endothelial cell, the basic pH of the extracellular fluid dissociates IgG from FcRn

Transcytosis.

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15
Q

Specific function of IgM, IgG and monomeric IgA

A
  • provide antigen-binding functions within the fluids and tissues of the body
  • Protect from blood-borne infection or septicemia
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16
Q

Dimeric IgA

A
  1. protects the mucosal epithelial surfaces
  2. Made by plasma cells in the lamina propria, but needs to be transported acorss the epithelium
  3. Dimeric IgA (not monomeric) binds to a receptor on the basolateral surface of the epithelial cells called the Poly Ig Receptor
  4. Facilitates trancytosis of IgA.
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17
Q

Poly Ig Receptor

A

Specific for IgA dimers and IgM pentamers

Found on the basolateral surface of the epithelial cells.

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18
Q

IgA + Poly Ig receptor

A
  1. binding of IgA to a receptor on basolateral face of epithelial cell
  2. receptor mediated endocytosis of IgA
  3. Transport of IgA to apical face of epithelial cell
  4. Receptor is cleaved, IgA is bound to mucus through the secretory piece (lumen)
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19
Q

Multiple functions of dimeric IgA

A
  • IgA can export toxins and pathogens from the lamina propria while being secreted
  • IgA is able to bind and neutralize antigens internalized in endosomes
  • Secreted IgA on the gut surface can bind and neutralize pathogens and toxins
  • Secrted IgA binds pathogen on M-cell surface and takes it to lymphoid tissue
  • secreted IgA picks up antigen in the endosomes of the M cell and takes it to lymphoid tissue
20
Q

antibodies in our blood

A

IgG, IgM, monomeric IgA

21
Q

antibodies in our respiratory system, digestive system, urogential tract

A

dimeric IgA

All these places are lined with mucosal epithelia.

22
Q

only isotype that can cross the placenta

A

IgG

23
Q

primary form of antibody found in breastmilk

A

Dimeric IgA

24
Q

an infants first year of life:

A

declines in maternally transferred antibodies coupled with development of their own IgM, IgG, IgA.

  • while they are in utero, the fetus recived passivly transferred maternal IgG. declines within about 9 months
  • 3 months - 1 year = transient low IgG levels (developoing its own IgG)
  • first antibody to appear in a babys life: Newly synthesized IgM
25
Q

Neutralization

A

Antibody interfering the interaction between the virus and its preferred receptor on the cell surface
- may be receptor or ligand
- virus prefers to a specific host cell protein.

Ex: IgA binds to virus which prevents it to bind to a receptor/ligand on cell surface leading to virus not infecting the individual.

26
Q

Toxin Neutralization

A
  1. toxin binds to cell surface receptor
  2. Endocytosis of toxin:receptor complex
  3. Dissociation of toxin to release active chain which poisons cell

The toxin wants to bind the receptor in order to go through endocytosis of the cell and release toxins.

  1. Neutralizing antibody blocks binding of toxin to cell surface receptor

^^ this happens if an antibody is able to prevent the toxin from binding to receptors on the surface

27
Q

antibodies against S. pyogenes F protein inhibit its ability to function as an adhesion to cause disease; neutralization

A

Neutralization:
- Child with anitbodies against S. pyogenes
- Antibodies prevent the attachment of bacteria to the tissues; most bacteria are swept to the gut
- Bacterial population is limited and kept as a steady state; child remains healthy

Disease:
- sister without anitbodies against S. pyeogenes
- bacteria stay in the pharynx and multiply
- bacterial population expands out of control and damages its environment; sister suffers from sore throat

28
Q

Complement fixation

A

Pentameric IgM is a perfect ligand for C1q
- initiates the classical pathway
- IgM and C1 are closely related, and if one is missing, ones complement system would be impaired.

(10 antigen binding sites)

29
Q

Binding of at least two molecules of IgG to pathogen or particle is required for complement fixation

A
  1. IgG molecules bind to antigens on bacterial surface = C1q binds to two or more IgG molecules and initiates complement activation
  2. IgG molecules binds to soluble multivalent antigen = C1q binds to soluble immune complex and initiates complement activation
30
Q

Immune complexes

A

Protein complex formed by binding of antibodies to soluble antigens.

  • size of immune complex is dependent on the concentration of antigen and antibody
  • large complex - often coated with complement and cleared by phagocytes
  • small complex - accumulate in small vessel walls where they can activate complement and cause damage
    1. renal podocytes, leads to damager of glomeruli (kidney disease)
31
Q

Patients with deficines in the ealry components of the complement cascade (C1)

A

cannot coat immune complexes with C4b and C3b, and cannot remove them

Leads to kidney damage.

32
Q

CR1 on an erythtocyte surface binds C3b tagged immune complex

A

Erythrocyte carries immune complexe to the liver or spleen where it id detached and taken by a macrophage

33
Q

Opsonization

A

Clearing of extracellular bacteria

34
Q

Important receptor in Opsonization

A

FcgammaR1

specific for IgG

35
Q

FcyR1

A

high affinity receptor for IgG1 and IgG3

  • FcyR1 binds the lower hinge and CH2 of IgG3
  • IgG3 bound to FcyR1 binds antigen
36
Q

Allergic and anti-parasite responses

A

IgE

37
Q

IgE

A

IgE binds to mast cells thrrough FcER1 (Fc epsilon receptor)

mast cells are already decorated with IgE on their surface. The interaction between IgE and Fcepsilon = high affinity receptor

38
Q

granules of mast cells

A

contain histamine and other inflammatory mediators
- multivalent antigen cross links IgE antibody bound at the mast cell surface causing the release of granule contents

39
Q

Good way to kill mutlicellular parasites

A

Eosinophils, mediates by IgE and Fcreceptor expressed on eosinophils

40
Q

Antibody-dependent cellular toxicity (ADCC)

A
  • NK cells can kill cells coated with IgG1 or IgG3, mediated through FcyRIII (CD16)
  • influenza infected cells can express viral glycoproteins which can be recognized by these IgG molecules, lead to ADCC
  • this is the mechanism of action of the anti-B Cell tumor drug Rituximab
41
Q

ADCC pathway

A

killing of antibody coated cell

42
Q

Activation

A

FcyR1
FcyR3-B

43
Q

High affinity

A

FcyR1 - binds gamma and is the major receptor for opsonization

44
Q

Low affinity

A

FcyR3-B - CD16 (NK cells)

FcyR2-B

45
Q

Inhibition

A

FcyR2-B (Naive B cells that prevent them to participiate in secondary responses)

46
Q

pH dependent

A

FcRN

47
Q

Increased Ig half life

A

FcRN

Immunology (18 decks)

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