B cell immunity - part 2 Flashcards Preview

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Flashcards in B cell immunity - part 2 Deck (35)
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1
Q

What B cells initiate the secondary immune response?

A

Memory B cells

2
Q

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

A

Yes

3
Q

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

A

more

more

4
Q

The memory responses produce more of what?

A

More long-lived plasma cells and more memory B cels

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

6
Q

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

A

Lipids and polysaccharides

7
Q

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

A

short-lived plasma cells only

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

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

10
Q

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

A

IgM

11
Q

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

A

No long term memory

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

13
Q

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

A

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

14
Q

Which antibody type is the first one produced in newborns?

A

IgM

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

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.

A

IgA

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
Q

What is the gold-standard for vaccines?

A

Its ability to neutralize a virus - will not pass clinial trials without this capability

26
Q

How do Abs trigger phagocytosis?

A

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
Q

What antibodies are present in the baby before birth? What does it change to?

A

IgG - can cross placenta

IgA - through breast milk

28
Q

Why do newborns have low antibody levels?

A

Small thymus - low levels of T cells - may not get full activation of B cells.

29
Q

When do newborns have the highest risk for infection? Why?

A

6 months - lowest antibody levels here

30
Q

When do children have increased risk for infection?

A

around 3 months to 1 year

31
Q

Agammaglobulinemia is a proble with what?

A

Problem with lymphoid progenitor cells, in which they do not develop into B cells within the bone marrow

32
Q

How are B cell defects usually treated?

A

Administration of purified IgG pooled from thousands of donors

33
Q

Why does a patient with agammaglobulinemia need recurrent treatments?

A

antibodies are proteins and thus get digested and lost over time.

34
Q

Why does agammaglobulinemia appear at around 10 months of age?

A

Passive immunity wears off in child since maternal antibodies get metabolized by then

35
Q

Why does a person suffering from agammaglobulinemia get recurrent bacterial infections?

A

Because B cells target extracellular pathogens