Humoral Immunity (Bowden) Flashcards

1
Q

Humoral Immunity

A

bracnh of adaptive mediated by Ab produced by plasma cells. principal defense against extracellular pathogens

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2
Q

Where are the Abs produced by plasma cells and where are they functional

A

produced in lymphoid tissues and organs. function is at distant sites

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3
Q

What mediates the effecter functions of Abs

A

The Fc region of isotypes

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4
Q

What triggers function of Ab

A

binding of Ab to Fab (Variable) regions on isotypes

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5
Q

3 general schematics of Ab function

A

Neutralization- prevents bacterial adherence
Opsonization- promotes phagocytosis
Complement activation- lyses some bacteria

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6
Q

Which classes of Ab can do neutralization

A

any of them. only requires binding to Ag- higher affinity the better.

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7
Q

Which mechanism do vaccination Ab work

A

neutralization

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8
Q

What regions of Ab promote phagocytosis and deliver the signals

A

Fc receptors

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9
Q

What cells are main responders to viruses

A

NK

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10
Q

Describe the method of NK binding. or Ab dependent cell cytotoxicity ADCC

A

NK bind Ab coated cell by Fc R and destroy cells

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11
Q

IgE mediated Rxns

A

IgE binds Fc R on mast cells and eosinphils.

When Ag binds- degranulation of cell occurs

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12
Q

What is FcRn

A

Fc neonatal R for transporting IgG across placenta

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13
Q

Why is IgG more important than IgM against bacterial infection

A

IgG has higher affinity and not only does it activate C’ cascade but it also can bind Fc on phagocytes

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14
Q

how many types of Hyper- IgM immunodeficiency exist

A
5 all are genetic defects
inability to switch class form IgM
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15
Q

X linked Hyper IgM immunodeficiency HIGM has what defect

A

CD40L expression.

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16
Q

sequelae of HIGM

A

neutropenia, failure to thrive, thrombocytopenia and anemia

17
Q

What will the assay testing cells binding to CD40 in patients with HIGM look like

A

much much fewer cells bind

18
Q

What will the assay testing cells binding anti-CD25 look like in patients with HIGM

A

normal because still binding IL2

19
Q

Describe HIGM combined immunodeficiency

A

CD40 also on macrophages and monocytes and DCs and platelets and epithelium- impaired handling of opportunist pathogens- less efficient killin

20
Q

What Ag response is okay in xlinked HIGM patients

A

Tindependent because doesn’t rely on CD40

21
Q

Why are there Ab to blood group Ag but not to tetanus in patients with HIGM

A

cross reactive sugars of A and B don’t need Tcell help. so T independent Ag reaction
Toxin in tetanus needs T help

22
Q

Tx for HIGM, mechanism?

A

intravenous Ig (IVIG) engages inhibitory FcR on B cells and possibly dendritic cells- suppresses immune system

23
Q

Cyroglobinuria

A

precipitation of ICs at below 37 Celsius

Chronic infection can lead to Immune complex disease. Immune complexes may become immunogenic themselves.

24
Q

What is rheumatoid factor + indicative of

A

patient making IgM to their own IgG

25
Q

Where are ICs usually accumulating in body

A

glomerulus of kidney- too large to filter

26
Q

Polyclonal B cell Response

A

by monoclonal Abs- extended Ag stimulation can lead to autoimmunity

27
Q

Short term effects of a hepatitis infection

A

cryoglobinuria and vasculitis

28
Q

more chronic effects of Hep C infection

A

immune mediated disorders

29
Q

What can occur in non-treated Hep C infection

A

B cell malignancies
Hepatocellular carcinomas
Thyroid cancer

30
Q

What can IC promote when deposited in wlal of blood vessels

A

activate C’ releasing C3a and C5a that will recruit leukocytes to area–>vasculitis

31
Q

Why would a monoclonal Ab against CD20 work for patients with cryoglobinuria

A

CD20 on B cells- anti Ab will target for B cell death