Humoral immunity and antibodies Flashcards

1
Q

Describe the activation of naive B cells

A
  • Similar to T cells it needs 3 signals
  • 1st= antigen binds to surface and is internalised then presented
  • 2nd= Antigen specific T cells bind to B cell, MHC 2 and CD4 and TCR all bind together
  • 3rd= Th2 cell releases co-stimulatory cytokines which bind to B cell
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2
Q

What happens once a B cell is activated?

A
  • Becomes a lymphoblast and undergoes class switching
  • Clonal proliferation
  • Formation of memory cells
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3
Q

Briefly list the stages of naive B cell activation

A
  • Binding of antigen to surface IgM/ IgD of B cell
  • Internal processing of antigen and presentation to Th cell via MHC 2
  • Molecular stabilisation of complex (CD4)
  • Th2 cytokine release (IL-4, IL-5)
  • Proliferation of B cell clone, plasma cell formation and Ig production increases.
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4
Q

How do you identify a plasma cell on a microscope slide?

A
  • Acentric nucelus

- Found in tissues/ LN not normally blood

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5
Q

Describe the activation of memory B cells

A

-Still require signals and help from Th2 cells to be activated

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6
Q

Describe the characteristics of memory B cells

A
  • Have much faster antibody synthesis
  • Increased affinity to Ag
  • Increased expression of MHC class 2 and costim molecules
  • Interact with armed t cells at lower Ag dose
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7
Q

What are the different regions of an Ig?

A
The Fab region= antigen binding site
The Fc (constant) region= determines biological activity. SIGNALLING.
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8
Q

What are the effects of Ag-Ab complex formation?

A
  • Opsonisation by complement (phagositation)
  • Binding to FcR on phagcytes (phagocytosis)
  • Persistence can damage organs (Type 3 hypersensitivity)
  • Crosslinking of IgE (mast cell degranulation)
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9
Q

What are the effects of the antibody binding to antigens on cells?

A

-Recognition by NK cells leading to ADCC

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10
Q

What are the effects of antibody on surface of a B cell binding to antigen?

A

Exogenous antigen presentation to Th2 cells, promotes plasma cell formation

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11
Q

What determines which class (isotype) the antibody is?

A

-The carbohydrate pattern of the constant region

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12
Q

Describe the primary and secondary immune responses

A
  • Primary: shows severe clinical signs,low magnitude, initiated in local LN, primary/ naive IR that largely involved IgM production, memory cells established
  • Secondary: memory cells present so clinical signs lessened, higher magnitude, initiated in local lymphoid tissues, IgM to IgG.
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13
Q

Where will you mainly find IgA?

A

Mucous membranes

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14
Q

Where will you mainly find IgG?

A

Serum and transudates into tissues

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15
Q

What does the presence of IgM indicate?

A

Acute phase of the antibody response to an antigen/ pathogen

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16
Q

Describe passive immunity

A
  • In neonates, colostrum ingested (12-36hrs post birth)
  • After this the gut is no long patent to transfer of antibiotics
  • ## Maternal antibodies in colostrum either remain high in gut (IgA) or transferred across gut epithelium (IgG).
17
Q

Describe the contents of colostrum

A
  • IgG (major component)
  • IgA (protects gut epithelium against bacterial invasion)
  • IgM/ IgE
  • Cytokines
  • Trypsin inhibitors
  • Lymphocytes (mainly T cells)
18
Q

How is IgG transported across gut epithelium in neonates?

A

-IgG transport protein (FcRn) expressed on gut epithelium
-2 molecules of FcRn bind one molecule of IgG
-Bind via Fc portion of IgG
-Endocytosis to reach local capillaries
(ACTIVE TRANSPORT)
- Can also transudate across

19
Q

List some factors that influence success of passive immunity

A
  • Type of placenta
  • Infection/ vaccination record of mother
  • Maternal immune response to vaccines
  • Quality/ quantity of colostrum
  • Number of young
20
Q

Which placental types have no transfer of IgG and so the neonates are completely reliant on colostrum?

A
  • Syndesmochorial (calf, lamb)

- Epitheliochorial (foal, piglet)

21
Q

What tests can you use to measure Ig transfer?

A
  • Latex agglutination

- Turbidity test

22
Q

What is serconversion?

A

The increase in titres of antibody from baseline levels. Commonly used diagnostically.