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Pathology Summer 2020 > Humoral Immunity > Flashcards

Humoral Immunity Flashcards

1
Q

Describe what an Ab looks like?

A

Has 2 heavy chains (Fc) region and inner arms.
Outer arms are light chains.
The bottom half is all constant and the upper paratope regions are variable.
Above the Fc region is the Fab region (Ag binding fragment)

4 polypeptide chains.
5 classes

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2
Q

Th1 helper cells do what?

Th2 helper cells do what?

A

Th1 activates CD8

Th2 activates B cells

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3
Q

Where are B cells made and mature?

A

Made and mature in hematopoietic bone marrow. Usually flat bones including the ileac crest of hips, top of femur, sternum, vertebrae and ribs.

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4
Q

B cell receptor complex

A

Antigen recondition molecule (usually IgD) and 2 accessory intracellular signaling molecules.

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5
Q

B cell clonal selection

A
  1. Antigen binds B cell. B cell phagocytes, processes, and presents epitope on MHCII.
    2a) epitope + MHCII of B cell will bind with T helper cell receptor.
    2b) Additionally, there will be a co-stimulatory signal from the t helper cell.
    2c) Cytokines will be released from T helper cell to signal B cell and signal Th2 formation.
  2. Now B cell has received the 3 signals to proliferate, class switch, and produce Ab.
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6
Q

When does class switch occur?

A

Occurs at time of activity activation of B cell by previously known antigen- only happens once.

If B cell is first activated and has never encountered an Ag before, the B cell will only produce IgM Ab and cannot class switch until later exposures.

Fetal cells cannot class switch

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7
Q

What determines which Ab the B cell class switches to?

A

Cytokine signals

Type/amount of antigen

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8
Q

What changes during the class switch? and what can the Antibodies class switch to?

A

Constant regions of the heavy chains change but Ag specificity remains the same.

A, E, G, or M. Cannot switch to D bc thats what is on the surface of B cells.

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9
Q

T-independent antigens

A

A BIG, repetitive identical antigenic determinant, antigen binding the B cell can activate the B cell without contact to TCR/costimulatory signals/cytokines.

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10
Q

Can you get a class switch with T-independent antigens?

A

No- due to no costimulatory or cytokine signal from Th2

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11
Q

Indirect and direct antibody functions

A

Indirect:
Complement activation
Opsonization
ADCC (antibody dependent cell mediated cytotoxicity)

Direct:
Neutralization
Agglutination
Precipitation

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12
Q

Indirect Ab function: Complement activation

A

Classical pathway is activated by Ab binding antigen. This activates C1 to start the cascade. Will result in MAC and pathogen death

Requires prior Ab response ?

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13
Q

Indirect Ab function: Opsonization

A

Ab will bind Ag to the Fab region. The Fc region of the Ab can bind the Fc receptors on phagocytes. The phagocytes will eat the Ag that the Ab is bound to

Requires prior Ab response ?

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14
Q

Indirect Ab function: ADCC

A

Used to destroy large organisms, many viral infected cells, or many cancer infected cells.

FcR on NK/MO/eosinophil cells will bind Fc region of Ab that is bound to Ag. NK will then phagocytose the Ab and large organism or cell it is attached to.

Requires prior Ab response!

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15
Q

Direct Ab function: Neutralization

A

Ab binds free floating toxins or viruses before they have the chance to bind to cells.
Involved in vaccines. Ex: tetanus vaccine produces Ab against the toxin.

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16
Q

Direct Ab function: Agglutination

A

ex uses IgM, has high valency. Clumping holds invaders still until immune cells can come in and destroy.

This process is for large, whole cells.

17
Q

Direct Ab function: Precipitation

A

Ab bind to small, water soluble molecules floating in solution and makes them insoluble, pulling them out of the solution so other immune cells can come clean it up.

18
Q

IgM

A 
Largest
Pentamer stabilized by J Chain 
10 valency 
First Ab produced during the primary response
Synthesized during fetal life
19
Q

First Ab produced during the primary response and fetal life

A

IgM

20
Q

IgG

A

Most abundant class (80-85%)
Transported across the placenta by active transport to provide passive immunity.
Four classes- IgG1-4

21
Q

Which Ig can be transported across the placenta?

A

IgG

22
Q

Two types of IgA

A

IgA1: Predominantly in the blood.
IgA2: Predominantly in mucosal secretions.

23
Q

IgA

A

Dimers anchored by J chain and secretory piece (prevents bacterial enzymes from degrading Ig)

24
Q

Which two Ig are stabilized by J chains?

A

IgM and IgA

25
Q

Secretory immune system in which tissues and secretions?

A

Lymphoid tissues throughout the body.

Present in tears, sweat, mucous, saliva, and breast milk.

26
Q

IgE

A

Least concentrated Ig class in CIRCULATION
Binds to surface of Mast cells and basophils.
Defender against parasites.
Mediator of many common allergic responses.
Atopic ppl have more IgE

27
Q

IgE activation starting with APC binding parasite Ag

A
  1. APC binds parasite AG and presents to Th2 cell.
  2. Th2 cell activates B cells to release IgE
  3. IgE will settle on mast cells. Once the Ag binds IgE fab region, Mast cells will degranulate.
  4. Degranulation of mast cells releases ECF-1 (eosinophil chemotactic factor-A) and histamine.
  5. This results in diapedesis of eosinophils that follow chemotactic signals to the parasite.
28
Q

IgD

A

Low concentration in blood

Found on the surface of B cells - function as receptor for B cell

29
Q

Primary humoral immune response

A
  1. Exposure
  2. Long lag period.
  3. IgM concentration increases
  4. Then IgG concentration increases (class switch) but doesn’t reach as high of concentrations as Igm.
30
Q

Secondary humoral immune response

A
  1. Exposure
  2. Short lag period.
  3. IgG concentration skyrockets
  4. At about the same time ^^, IgM concentrations increase, but to a much much lower degree.

Immune response is quicker, stronger, and stays on longer.

31
Q

T cell primary and secondary immune response

A

Primary:

  1. Infection
  2. 1 week until effector expansion occurs (proliferation)
  3. 7-30 days pass before memory cells are made.

Secondary:
Response is quicker and larger due to memory cells.

32
Q

Fetal/neonate immunity:

A
  1. Ab function is deficient. Passive immunity provided by material Ab
    - IgG crosses placenta
    - IgA in breast milk
33
Q

Elderly immunity:

A
  1. Decreased T cell activity- thymus atrophies over life.
  2. Decreased circulating B memory cells.
  3. Decreased MO activity= more Ab:Ag complexes= precipitations and problematic.
  4. Tolerance system fails. Increase in auto Ab
34
Q

Cell that bridges from innate to adaptive immune system

A

Dendritic. Contacts Ag in epithelium and brings to secondary lymphoid tissues for clonal selection.

Pathology Summer 2020 (19 decks)

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