Addaptive Immunology Flashcards

1
Q

Adaptive immune system function

A

Creates immune response to specific antigen

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2
Q

What is an antigen

A

Foreign protein or other molecule that is the target of an immune response

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3
Q

Adaptive immunity cells

A
  • antigen presenting cells (APCs) present antigen complexed with MHC (major histocompatability) class II proteins on cell surface
    Occurs in lymph nodes, leads to cytokine signaling and lymphocytes activation
  • T lymphocytes
    Helper T cells (CD4+) or cytotoxic T cells (CD8+)
  • B lymphocytes
    Memory B cells, plasma B cells
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4
Q

B lymphocytes function

A

Memory B cells- secondary immune response to same antigen
Plasma B cells- make antibodies, bind to specific antigen

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5
Q

Two types of adaptive immunity

A

Humoral immunity- fights invaders outside cells (bloodstream)
- bacteria and toxins
- involves plasma B and antibodies
Cellular immunity- attacks antigens found inside cells
- virus, fungi, parasites
Involves cytotoxic T cells and natural killer cells

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6
Q

What happens when B cells activate

A

Undergo clonal expansion (proliferation) producing plasma cells and memory cells (long lived)

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7
Q

What can activate B cells

A

T independent antigens activate B cells directly
T dependent antigens require activation of helper T cells that produce cytokines to activate B cell indirectly
T-independent = direct activation
T- dependent - indirect activation

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8
Q

What determines t-dependent or independent

A

Type of antigen
Amount present

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9
Q

Where do antigen-antibody complexes go

A

Cleared by complement cascade or
Liver or spleen

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10
Q

What is co stimulation of B cell

A
  1. Antigen bind to B cell receptor
  2. T cell receptor interacts with antigen presenting MHC class II protein
    - two signals for B cell to become activate and mature into plasma cell
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11
Q

Why is co stimulation of B cell important

A

Two signals to all B cell activation and mature
Ensure that the B cell activation is required, not an oops with correct antigen binding or an oops with TCR binding to MHC II
Prevent immune overdrive

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12
Q

Plasma B cell creation stages

A
  1. Stem cells differentiate into mature B cells, each bearing surface immunoglobulin against specific antigen- checks that receptor shape doesn’t target body cells, and that it targets antibody effectively- after success CLONE EXPANSION of specific antibody
  2. B cell encounters specific antigen and proliferates (into plasma and memory)
    3a. B cells proliferate into long lived memory cells (these memory cells can be used at a later date, stimulated by antigen, become plasma cell)
    3b. Plasma cells secrete antibodies into circulation
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13
Q

Acquired immunity: antigen-specific responses

A

All responses result in antibody binding to antigen
1. Agglutination: clumping of bacteria so all in localized region, easy antibody pick up
2. Opsonization: coat antigen with multiple antibodies enhances phagocytosis, easier for macrophage to engulf
3. Neutralization: blocks adhesion of bacteria/virus to mucosa and blocks attachment of toxin. Antibodies bind to virus, bacteria, toxin
4. Antibody-dependent cell-mediated cytotoxicity: used for parasites (large bad cells) can’t engulf. Antibodies coat the parasite allowing macrophages, eosinophils, natural killer cells to destroy using lytic enzymes, perforin
5. Activation of complement: protein binds to antibody on bacteria, put holes in bacteria cell wall, cause inflammation and cell lysis

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14
Q

Where are T cells produced and matured

A

Produced in red bone marrow
Mature and undergo ‘thymic selection” in the thymus

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15
Q

Function of T cell receptor

A

Antigen binds- every T cell has one specific antigen

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16
Q

How are T cells activated

A

Antigen presenting cell (APC) that has antigen complex with MHC II- could be B cell in t-dependent, dendritic cell, infected body cell

17
Q

How are different T cells made and what MHC do they interact with

A

CD4+ and CD8+ are receptors

CD4+ T cells become helper T cells. Interact with MHC II present on APCs or MHC I on infected cells
CD8+ T cells become cytotoxic T cells. Interact with MHC I found on all nucleated cells of body (not RBC)

18
Q

What other things can helper T cells become

A

Memory T cells

19
Q

TH cell activation

A
  1. An APC encounters and ingests a micro-organism. Antigen is enzymatically processed into short peptides which combine with MHC class II molecules and are displayed on surface of APC
  2. TCR on surface of CD4+ helper cell binds to MHC antigen complex. TH cell or APC is stimulated to secrete co-stimulatory molecule. (Co-stimulatory molecule required to activate T cells that have not previously encountered antigen). Two signals activate TH cell produce cytokines
  3. Cytokines cause TH cell to activate
20
Q

TC activation

A
  1. Virus-infected cell or cancer cell (MHC class I body cells) produce abnormal endogenous antigens
  2. Abnormal antigen is presented on cell surface in association with MHC class I molecules. Binding of TH1 cell to MHC class I antigen presenting promotes secretion of cytokines
  3. Cytokines activate a precursor CTL which produces a clone of CTLs (cytotoxic T cell activation)
  4. CTL induces destruction of the virus-infected cell by apoptosis
21
Q

T cell precursor differentiation

A
  1. ? Somehow -> natural killer cells -> kill antibody coated cells or bacteria, MHC class I APC
  2. Migrate to thymus -> cytotoxic T cells -> kill MHC class I APC
  3. Migrate to thymus -> helper T cell -> bind to MHC class II APC or MHC class I antigen infected cell -> secrete cytokines that activate other immune cells
22
Q

Pathway of complement activation

A

Antibody binds to antigen and activates C1
C1 splits and activates C2 and C4
C2a+ C4b come together -> C3
C3 split into C3a + C3b (diff jobs)
C3a- function inflammation
C3b- function in cytolysis and opsonization (coating pathogen)

23
Q

Outcomes of complement activation

A

Cytolysis (apoptosis)
C3b activate C5
C5 split C5a + C5b
C5b activates C6
C6, C7, C8, C9 get together, form ring, enter pore -> apoptosis
Opsonization
C3b act like antibodies and coat. Makes life easier for macrophage/ phagocyte to locate and engulf
Inflammation
C3a binds to receptor of mast cells -> Histamine release
And
C3b -> c5 -> C5a + C5b -> C5a bind to receptors of mast cells -> histamine release

24
Q

What happens without immunity

A

Graph # of micro-organisms vs duration of infection (t)
- lacking innate - no physical/chemical barriers, huge increase in micro-organisms
- lacking adaptive - still have barriers working, but overtime invaders increase and no antibodies or T cells to remove them
- normal human graph a parabola- down as recovery

25
Q

Interferons creation and use pathway

A
  1. Viral RNA from an infected virus enters the cell
  2. Virus induces the host cell to produce interferon mRNA (IFN-mRNA) which is translated into alpha and beta interferons
  3. Interferons make contact with uninflected neighbouring host cells -> bind to plasma membrane or nuclear receptors. Interferons induce the cells to synthesize antiviral proteins (AVPs)
  4. AVPs degrade viral mRNA and inhibit protein synthesis (outcome- interfere with viral replication)
  • interferons made in infected cell
  • interferons make uninfected cell synthesize antiviral proteins
  • by the time cell becomes infected, AVP will degrade viral mRNA