B cell immunity - part 2 Flashcards

1
Q

What B cells initiate the secondary immune response?

A

Memory B cells

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2
Q

Do we still need a Tfh cell for the secondary response?

A

Yes

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3
Q

Memory responses are more protective as _____ B cells respond to protein antigen, leading to _____ Abs produced.

A

more

more

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4
Q

The memory responses produce more of what?

A

More long-lived plasma cells and more memory B cels

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5
Q

What are differences between the primary B cell response, and subsequent ones?

A

Primary response takes longer to initiate.
Primary response secretes IgM first, then other antibody types later; secondary response has an increased number of IgG, IgA and IgE earlier.
Secondary response is stronger than the primary response

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6
Q

What are non-protein antigens that B cells can bind to?

A

Lipids and polysaccharides

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7
Q

When B cells bind to non-protein antigens, what cell types are produced by clonal expansion?

A

short-lived plasma cells only

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8
Q

What is a major difference between B cells responding to protein antigens, and responding to non-protein antigens?

A

No Tfh cell input is needed when responding to non-protein antigens

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9
Q

Why are Tfh cells not needed when a B cell responds to a non-protein antigen?

A

Non-protein antigens have very high affinity for BCR

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10
Q

What are the only antibodies produced when responding to non-protein antigens?

A

IgM

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11
Q

What is a major downfall of the response to non-protein antigens?

A

No long term memory

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12
Q

IgD:
- levels in the blood?
Function?
Where are most of them found?

A

Low levels in blood
Ab function is unknown/ bind pathogens as BCR
Most remain bound to naive B cells

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13
Q

IgM:
- location?
- Key characteristic?
Main form?

A

Mainly found in blood
First antibody produced in primary immune response
Pentameric

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14
Q

Which antibody type is the first one produced in newborns?

A

IgM

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15
Q

IgA:

  • most abundant where?
  • what does it provide to a newborn? How is this accomplished?
A

Most abundant Ab in secretions (mucus, tears, saliva, breast milk)
Provides passive immunity to newborn; maternal IgA transferred to newborn via breast milk

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16
Q

IgA is mainly produced where?

A

MALT tissue

17
Q

These antibodies can cross the epithelial barrier and can protect us from invading pathogens or toxins that may be sitting in our mucosal membranes.

18
Q

IgE:

  • instrumental in immunity against what type of pathogen?
  • involved in which type of reaction?
A

Instrumental in anti-parasitic immunity

Involved in allergic reactions

19
Q

Increased serum IgE is generally indicative of what?

A

Either parasitic infection, or allergic reactions

20
Q

IgG

  • most abundant where?
  • provides what to newborns? How?
A

Most abundant antibody in blood and tissues

Provides passive immunity to newborn - maternal IgG is the ONLY isotope that can cross the placenta

21
Q

How do IgG antibodies enter infected tissues?

A

Via inflammation

22
Q

What are the mechanisms of antibody-mediated destruction of extacellular pathogens?
Which antibodies are involved?

A

Neutralization and Triggering phagocytosis

IgM, IgG, IgA

23
Q

What are the antibody titers in the serum (i.e. which is most abundant in the blood, to which is the least?

A

IgG, IgA, IgM, IgD, IgE

24
Q

What is neutralization?

A

Antibodies block a virus from binding to its target cell by binding to the virus’ surface and preventing it from entering the host cell

25
What is the gold-standard for vaccines?
Its ability to neutralize a virus - will not pass clinial trials without this capability
26
How do Abs trigger phagocytosis?
Ab binds to invading bacterium. Fc receptor on phagocyte binds to Fc region on the Ab. Fc region will trigger Fc receptor to internalize pathogen and cause phagocytosis
27
What antibodies are present in the baby before birth? What does it change to?
IgG - can cross placenta | IgA - through breast milk
28
Why do newborns have low antibody levels?
Small thymus - low levels of T cells - may not get full activation of B cells.
29
When do newborns have the highest risk for infection? Why?
6 months - lowest antibody levels here
30
When do children have increased risk for infection?
around 3 months to 1 year
31
Agammaglobulinemia is a proble with what?
Problem with lymphoid progenitor cells, in which they do not develop into B cells within the bone marrow
32
How are B cell defects usually treated?
Administration of purified IgG pooled from thousands of donors
33
Why does a patient with agammaglobulinemia need recurrent treatments?
antibodies are proteins and thus get digested and lost over time.
34
Why does agammaglobulinemia appear at around 10 months of age?
Passive immunity wears off in child since maternal antibodies get metabolized by then
35
Why does a person suffering from agammaglobulinemia get recurrent bacterial infections?
Because B cells target extracellular pathogens