Lecture 29: Infection and immunity Flashcards

1
Q

What factors affect infection and response to it?

A
  • Environmental
  • Social/epidemiological
  • Psychological
  • Genetic/lineage
  • Ontogenetic/personal history
  • Behavioural
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2
Q

What are the lymphocyte effector populations?

A
  • B Antibody production (B-lymph)
  • Antigen-specific cytotoxicity (CD8 T cells)
  • Natural killer activity (NK lymphocytes)
  • ADCC (K lymphocytes)

NK & K are functions of same subsets of cells. Manifest one or other depending on context of antigen presentation

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3
Q

What are the lymphocyte regulator cells?

A
  • Cytokine production (CD4 T lymph)
  • TH1 (Intracellular)
  • TH2 (Multi-cellular i.e parasites, allergens)
  • Treg (Regulatory T cells, down regulation)
  • TH17 (Mucosa and inflammation)
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4
Q

Describe antibody responses change between primary and secondary response:

A

Class switch from IgM to IgG controlled by T cells, needs CD40-CD40Ligand interaction

IgG much high conc. second time.

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5
Q

What happens in hyper-IgM syndrome?

A

No CD40-CD40Ligand interaction = No class switching to IgA, IgG, IgE

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6
Q

What are the microbial factors when it comes to infection:

A
  • Type of organism
  • Amount
  • Route of entry i.e Gut->Peyers Patches, Blood->Spleen
  • Virulence
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7
Q

What are the host factors that influence infection?

A
  • Integrity of the innate barriers
  • Adaptive immune competence
  • HLA, TCR and Ig genes
  • Previous exposures
  • Other infections
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8
Q

What factors influence immunity and infection?

A

Microbial and host factors

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9
Q

What can the lymphocyte populations be divided into?

A

Effectors and regulators

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10
Q

Write some notes on viruses and its antigens:

A
  • Lytic or integrated cycle
  • Capsid antigens
  • Internal structural components (HLA Class 1)
  • Metabolic products (HLA Class 1)
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11
Q

Write some notes on bacteria (and fungi) and its antigens:

A
  • Extracellular (S. aureus) or intracellular (M. Tuberculosis)
  • Structural components
  • Metabolic products or toxins
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12
Q

Write some notes on parasites and its antigens:

A
  • Large (multicellular) (slower)
  • Life cycle changes
  • Radical changes in antigenicity
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13
Q

What are the arms of the immune system?

A
  • Direct neutralisation by antibodies
  • Opsonisation and phagocytosis
  • Complement mediated effects
  • HLA restricted T cell mediated cytotoxicity
  • NK cell mediated cytotoxicity
  • Inflammatory and immunoregulatory cytokines
  • Antiviral cytokines (i.e interferons)
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14
Q

What do antibodies target?

A

Effective against antigens outside cells of body

  • Viruses
  • Toxins
  • EC bacteria
  • Parasites
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15
Q

What do cytotoxic T cells target?

A

Effective against intracellular protein antigens

  • Virus infections
  • Tumour cells
  • Transplanted organs
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16
Q

How does bacteria trigger the immune system?

A

PAMPS i.e LPS, peptidoglycans

Local inflammation

  • Vascular permeability changes
  • Phagocyte recruitment
  • Acute phase protein induction
  • Local temp changes

== Phagocytosis and compliment activation

17
Q

What is the effect of antibodies and compliment against bacteria?

A

AB and compliment

  • Prevent adherence or reduce mobility
  • Enhance bacterial destruction (complement)
  • Enhance phagocytosis (Opsonisation)
18
Q

How do bacteria avoid AB effects?

A
  • Capsule resistance i.e heamophilus influenzae

- Intracellular growth i.e mycobacterium tuberculosis

19
Q

Describe how cells decide on NK or K lymphocyte activity:

A

This population of cells have a Antibody receptor (CD16) (ADCC). In addition they have a killer activating receptor + killer inhibitory receptor. (NK activity)

If the KAR+KIR bind a normal cell, theres antigens for both. IF it binds a abnormal cell i.e infected or tumour (down regulated HLA1). Then only KAR is activated and the NK cell attacks the abnormal cell.

If an antigen is recognised by CD16 then it has ADCC activity.

20
Q

What cytokines enhance NK activity?

A

IL2 and IFN-gamma enhances activity.

21
Q

Describe the time profile of acute viral infections:

A
  • Interferon peaks first (Produced by infected cells to induce transient anti-viral state of neighbouring cells).
  • NK activity follows quickly and peaks in activity
  • Cytotoxic cells come last and antibodies.
22
Q

What are some pro-inflammatory cytokines and what do they do?

A

IL1, IL6, TNF-a

  • Induce acute phase proteins
  • Fever + Behavioural changes
  • TNFa triggered by bacterial LPS
  • Tissue repair: Bone reabsorption, fibroblast proliferation, collagenase synthesis, leukocyte adhesion.
  • T and B cell activation
23
Q

What is the role of chemokines in infection?

A
  • Aid chemotaxis

- Direct effector cell traffic

24
Q

What is the role of interferons in infection?

A
  • Induce transient antiviral state
  • Activate NK cell activity
  • Upregulate MHC expression (improves CD8 T cells killing)