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My Phase 2a > Immunology > Flashcards

Immunology Flashcards

1
Q

what are the main types of host defence

A
  1. intrinsic - always present and can be physical or chemical
  2. innate - induced by an infection e.g. interferon, cytokines, macrophages etc.
  3. adaptive - is tailored to a specific pathogen – T and B cells.
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2
Q

what is the difference between innate and adaptive immunity

A

innate you are born with and adaptive you acquire

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3
Q

what are the 2 main effectors in innate immunity

A
  • specialist macrophages [kupffer cells, dendritic cells, alveolar macrophages]
  • neutrophils
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4
Q

what are the precursor of alveolar macrophages

A

monocytes

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5
Q

what are neutrophils

A

a type of WBC

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6
Q

where are neutrophils made

A

in the bone marrow, making the myeloid cells.

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7
Q

what is a key component of neutrophils that helps with their function

A
  • They contain granules:
    • PRIMARY – myeloperoxidase, elastase, cathepsins, defensins
    • SECONDARY – receptors, lysozyme, collagenase
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8
Q

neutrophils are not involved in inflammation - T/F

A

False

  • neutrophils participate in the inflammatory response and protect against infection
  • They are present in blood at all times but are only activated when needed → generation of ROS
  • as the insult is removed and healing begins, the inflamm cells must be removed via
    • exudate
    • migration
    • apoptosis
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9
Q

what are the 7 functions of neutrophils

A
  1. identification of pathogen
  2. activation
  3. adhesion
  4. chemotaxis / migration
  5. phagocytosis
  6. bacterial killing -
    1. achieved via enzymes and ROS generation by NADPH oxidase complex
  7. apoptosis
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10
Q

which cells mediate adaptive immunity and by what mechanism?

A
  • B cells by humoral responses
  • T cells by cell-mediated responses
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11
Q

what is an antigen

A
  • a molecule able to induce a specific immune response from the host.
    • Can be proteins, polysaccharides, lipids, DNA etc.
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12
Q

what is an epitope

A

One antigen can have different epitopes – recognisable regions of the antigen

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13
Q

what are the 4 main types of T-cells

A
  1. Cytotoxic T-cells
  2. T-helper cells
  3. T-regulatory cells
  4. Memory T- cells
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14
Q

where are B and T cells made and where do they mature?

A
  • B cells:
  • made in the bone marrow
  • maturation begins in the bone marrow and ends in the spleen, lymph nodes
  • T cells
  • made in the bone marrow
  • Mature in the thymus
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15
Q

what are 3 key functions of adaptive immunity?

A
  1. specificity and diversity
  2. self- tolerance - recognition of self-antigens and elimination of autoreactive clones
  3. memory via signature BCRs and TCRs.
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16
Q

In what form do T and B cells recognise antigens?

A
  • B cells
  • B cell receptors recognise antigens in the native form AND when presented by antigen presenting cells.
  • T cells recognise antigens presented on MHCs on APCs
    • APCs include: dendritic cells, macrophages, B cells
17
Q

what is an antibody

A

a protein with a constant and a variable region

18
Q

describe cell-mediated immunity

A

t-cells can have CD4 or CD 8 expression

  • CD8
  • a cell that is infected presents the pathogen’s antigen on its surface via an MHC1 molecule
  • T-cells that fit the antigen, with CD8 expression, encounter and bind to MHC1 presenting cells
    • all nucleated cells have MHC1
  • this → activation of the T-cell → CD8 cytotoxic T-cell response.
  • CD4
  • an antigen presenting cell encounters a pathogen and presents the antigen on its surface via MHC2
  • the APC travels to the lymph node and presents to a matching T-helper cell with CD4 expression
  • this binding → activation and multiplication of the T-cells
  • T-helper cells and CD4 cytotoxic T-cells are produced
    • the helper cells
      • help B cells produce antibodies
      • form memory T-cells
      • form Regulatory T-cells to stop immun overreaction and help identify self-antigens
19
Q

Describe Humoral immunity

A
  1. the pathogen’s antigen binds to a matching BCR either in its native state or via and APC.
  2. the antigen is then taken up into the B cell by endocytosis and the antigen is presented on its surface via MHC2
  3. a follicular T-helper cell with a matching TCR binds to the antigen presented on MHC2 on the B-cell → activation of the follicular T-cell → production of helper factors
  4. helper factors activate the B-cell → plasma cell formation and memory B-cell formation.
20
Q

how are such variable BCRs and TCRs created

A
  • VDJ gene recombination
    • Variable, Diversity, Joining segments
  • this recombination process is very random → ⇡ diversity.
21
Q

what is somatic hypermutation and where does is occur?

A
  • after a matching BCR binds to an antigen it proliferates.
  • during proliferation loads of mutations occur in the binding regions of the BCR to increase affinity for the antigen → more efficient antibodies.
  • only occurs in B cells
22
Q

what is immune tolerance and how is it mediated?

A
  • immune tolerance is the bodies ability to not respond to the adaptive immunity system to avoid an overreaction.
  • T-reg cells are responsible for this by killing immune cells with receptors capable of binding to self-cells.
23
Q

how many hypersensitivity classes are there?

A

4

  1. Type 1: Allergy, anaphylaxis and atopy – IgE dependent acute response
  2. IgG binding to self antigens (autoimmune)
  3. immune complex diseases
  4. delayed type hypersensitivity reaction
24
Q

describe a type 1 hypersensitivity response

A
  • Type 1: Allergy, anaphylaxis and atopy – IgE dependent acute response
  • involved in conditions such as asthma, eczema and hay fever
  • IgE causes release of histamine from mast cells by activating FcεR1 receptor. → vasodilation and opening up of gap junctions
  • treated with antihistamines, steroids and avoiding triggers
    • effects seen immediately - within an hour
25
Q

describe a type 2 hypersensitivity response

A

IgG binding to self antigens (autoimmune)

  • cytotoxic
  • the immune system attack the body’s own cells
  • e.g.
    • effect seen in hours - days
26
Q

Describe a type 3 hypersensitivity response

A

Immune complex disease

  • A large scale immune response
  • complexes of IgG precipitate and can’t be cleared by macrophages
  • e.g. Farmers lung
    • effects seen within 7-10 days
27
Q

describe a type 4 hypersensitivity response

A

delayed hypersensitivity reaction

  • Type IV hypersensitivity is a T-cell-mediated hypersensitivity, meaning the inflammation and potential tissue damage is caused by either T helper cells (CD4+) or cytotoxic T cells (CD8+).
  • antibodies are not involved
  • e.g. tuberculosis
    • effects seen in day - weeks - months
28
Q

characteristics of IgG

A
  • most abundant antibody/ immunoglobulin
  • acts as an opsonin - binds to the pathogen and signals phagocytes towards it for phagocytosis
29
Q

characteristics of IgA

A
  • found on the mucosa surface
  • prevents pathogens from entering the body
30
Q

characteristics of IgE

A
  • involved in type 1 hypersensitivity reactions
  • seen in asthma, atopic dermatitis and hayfever
31
Q

characteristics of IgM

A
  • IgM is the first antibody secreted by the adaptive immune system
  • it activates complement
  • doesnt require t-cell help
32
Q

characteristics of IgM

A
  • IgM is the first antibody secreted by the adaptive immune system
  • it activates complement
  • doesnt require t-cell help
33
Q

Characteristics of IgD

A
  • helps mature B cells leave the bone marrow

My Phase 2a (35 decks)

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