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HUBS191 Immunology > Adaptive immune response > Flashcards

Adaptive immune response Flashcards

1
Q

dendritic cell

A
  • Antigen-presenting cell
  • take up fragments of microbes they have come across in the skin
  • Switches on adaptive immune system
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2
Q

antigen

A

Anything that has potential to be recognised by immune system

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3
Q

MHC-I (what it presents, where its expressed and whats it used for)

A
  • presents endogenous (intracellular) antigen.
  • Expressed on all nucleated cells
  • used for virally-infected cells
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4
Q

MHC-II (what it presents, where its expressed and whats it used for)

A
  • presents exogenous (extracellular) antigen.
  • Expressed only on antigen presenting cells
  • used for bacteria and virions that have not yet entered cells
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5
Q

MHC-I antigen processing

A
  • antigen is engulfed by cell directly into cytoplasm
  • Antigenic proteins are degraded to peptides in cytoplasm.
  • Peptides are imported into endoplasmic reticulum (ER).
  • Peptide loading of MHC-I takes place in ER
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6
Q

MHC-II antigen processing

A
  1. phogocytosis of exogenous antigen
  2. antigenic proteins are degraded in acidic phagolysosome
  3. peptide loading of MHC-II takes place in a phagolysosome
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7
Q

trafficking of dendritic cells into lymph node

A

when dendritic cells phagocytose antigen, they migrate from peripheral tissues to lymph node where they meet T cells for T cell activation

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8
Q

how are CD4 T cells activated

A
  • TCR recognises MHC-II + peptide
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9
Q

CD8 T cell

A
  • TCR recognise MHC-I + peptide
  • Develops into ‘cytotoxic T lymphocyte’ (CTL) due to recognition of MHC-I and help of cytokines
  • Cytokines produced by CD4 T cells help CD8 T cells become activated
    • If CD4 didn’t control CD8 activity, we would have autoimmune diseases as CD8 destroy our own cells
  • Cause apoptosis of virally-infected cell displaying MHC-I (MHC-I is very widely expressed throughout body)
  • Destroy pathogen by destroying its environment
  • Mainly target viral and cancer cells
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10
Q

B cell differentiation

A
  1. Native antigen attaches to B cell receptor (BCR) - IgM and IgD
  2. Helper T cell attaches to antigens presented by the B cell MHC-II (this causes cytokines to be released from helper cell)
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11
Q

T cells

A
  • lymphocytes that arise in bone marrow and mature in thymus (primary lymphoid organ)
  • each T cell expresses unique TCR along with co-receptors (either CD4 or CD8)
  • recognise MHC/peptide complexes
  • types of MHC depends on type of co-receptor
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12
Q

T cell development

A
  • T cells develop in the thymus (primary lymphoid organ)
  • Immature T cells have identical T cell receptor genes
  • Immature T cells under TCR gene rearrangement – producing mature (naïve*) T cells that express a variety of unique antigen receptors
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13
Q

CD4 T helper cells

A
  • Recognise MHC-II/peptide complexes (from antigen-presenting cells)
  • Produce cytokines which ‘help’ CD8 T cells to become cytotoxic
  • Bind to MHC-II/peptide complexes on B cells to activate them. This ‘helps’ B cells to make antibody
  • Bind to MHC-II/peptide complexes on macrophages to upregulate their function
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14
Q

CD8 cytotoxic T cells

A
  • Recognise MHC-I/peptide complexes
  • Receive ‘help’ from CD4 T cells (in the form of cytokines)
  • Develop into cytotoxic T lymphocytes, which bind to MHC-I/peptide complexes on virally- infected cells and induce their cell death via apoptosis. It does this by producing perforin (forms pores in cell membrane) to allow granzyme (induces apoptosis) to enter
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15
Q

how are CD8 cells activated

A
  1. recognition of MHC-I on any nucleated cell
  2. help from CD4 T cells via cytokines
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16
Q

clonal selection

A
  • When naïve B cells bind their antigen, they do so with high affinity. In the secondary lymphoid organs, these B cells are selectively expanded (stimulated to undergo cell division) in order to provide enough cells to fight of that specific infection.
  • Both plasma cells and memory cells are created by this cloning process
17
Q

function of anitbodies

A
  1. neutralisation - bind to surface structures on microbes to block ability to attach to host cells. also bind to toxins to prevent action
  2. opsonisation - bind to surface of microbes so they’re more recognisable to phagocytes. agglutination increases efficiency of uptake by phagocytosis
  3. complement activation - antibody bound to surface of pathogens activates complement cascade via classical pathway
18
Q

antibody classes

A
  • IgG
  • IgA
  • IgM
  • IgE
  • IgD
19
Q

IgG: number of subunits, distribution, and function

A
  • Monomer
  • Most abundant Ig class in blood
  • Targets viruses and bacteria; Opsonises and neutralises; Only Ig class that crosses the placenta – confers ‘passive immunity’ on the foetus
20
Q

IgA: number of subunits, distribution, and function

A
  • monomer in blood, dimer in secretions (joined by J chain)
  • present in secretions such as tears, saliva, mucous and breast milk
  • targets viruses and bacteria; defence of mucous membranes; confers ‘passive immunity’ on infant
21
Q

IgM: number of subunits, distribution, and function

A
  • Pentamer in blood (joined by J chains), Monomer as BCRs
  • First Ig class produced after initial exposure to antigen; Expressed on naïve B cells – as BCRs
  • Targets extracellular bacteria; Activates complement; Together with IgD, acts as antigen receptors on B cells (BCRs)
22
Q

IgE: number of subunits, distribution and function

A
  • Monomer
  • Present in blood at low concentrations
  • Immunity to multicellular parasites; Implicated in allergic reactions (e.g. anaphylaxis)
23
Q

IgD: number of subunits, distribution and function

A
  • Monomer
  • Expressed on naïve B cells – as BCRs
  • Together with IgM, acts as antigen receptors on B cells (BCRs); Specific function unknown
24
Q

class switching

A
  • involves B cells switching their class of immunoglobulin, but maintaining their specificity for a specific antigen
  • Structurally this involves changing of the constant regions (specific to Ig class) while keeping the variable regions (specific to antigen) the same
25
Q

timeframe of immune responses and antibody involved

A
  1. Primary immune response: takes 1-2 weeks before sufficient antibody is produced to eliminate a pathogen (relatively small amount of antibody produced, mainly IgM)
  2. Secondary immune response: relies on memory B cells, is fast (2-3 days) and mainly produces IgG. This is the basis of the success of vaccination (vaccination produces a pool of memory B cells so that when you get the actual infection, you have a fast response).
26
Q

adaptive immune response to viruses

A
  1. virally-infected host cells present endogenous on MHC-I
  2. CD8 T cells recognise endogenous antigen on MHC-I
  3. APCs (dendritic cells) phagocytose virally infected cells and present exogneous antigen on MHC-II
  4. CD4 helper T cells recognise exogenous antigen on MHC-II
  5. CD4 celper T cells release cytokines which allow CD8 T cells to turn into cytotoxic T cells (CTL)
  6. CTL’s release perforin (forms pores in virally-infected cells presenting MHC-I) and granzyme (induces apoptosis)
27
Q

vaccine function and components

A
  • Help prime immune response for future exposure to a viral pathogen
    1. Antigen - specific molecule that the immune system may recognise (made using heat-killed, attenuated or recombinant viral protein)
    2. Adjuvant - helps to enhance the immune response against the antigen
28
Q

central tolerance

A

Prior birth, our body goes through all our lymphocytes and deletes those which recognise antigens of our own body

  • Either destroyed
  • or re-edit receptors on lymphocytes
  • Or developed into CD4 helper T cells which regulate lymphocyte action
29
Q

immunoprivileged sites

A

Body creates special zones where immune system cannot go

  • e.g in testes - prevents sperm being killed off in our own body
  • e.g. eye - cornea transplants can take place
30
Q

peripheral tolerance

A

lymphocytes which recognise self-antigens which evade central tolerance mechanisms either have their receptors removed (anergy), undergo apoptosis, or are suppressed by regulatory T cells

31
Q

why are transplants rejected

A
  1. direct recognition: when APC of transplanted organ takes up and presents foreign peptide (its own) to host T cell - triggers immune response
  2. indirect: APC of host goes into kidney and takes up and presents foreign peptide to host T cell
32
Q

type 1 hypersensitivity

A
  1. first exposure
  2. allergen bind directly to B cell
  3. B cell matures and T helper cell causes B cells to produce IgE antibodies
  4. IgE binds to constant region on mast cells so the act as receptors
  5. on repeat exposure to allergen, allergen binds to mast cells with IgE receptors
  6. activation of mast cell - large release of cytokines and mediators
33
Q

primary lymphoid organs

A

where lymphocytes are made and mature:

  • thymus and bone marrow
34
Q

secondary lymphoid tissue

A

where lymphocytes congregate:

  • spleen and lymph nodes

HUBS191 Immunology (2 decks)

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