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Microbiology And Immunology > Autoimmunity > Flashcards

Autoimmunity Flashcards

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1
Q

Examples of autoimmune disease
State the ways autoimmune diseases are present?

A

Systemic or organ-specific

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2
Q

State 2 examples of organ-specific autoimmune diseases?

A
  • Graves disease: over activation of TSH receptors in thyroid -> bulging of eyes
  • Type 1 diabetes: Targets insulin producing cells of the pancreas
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3
Q

State and describe an example of a systemic autoimmune pathology?

A
  • Systemic lupus erythematosus
  • Multi-system disease
  • Characterised by autoAB to nuclear antigens (dsDNA) -> Relapse + remission of disease
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4
Q

Basics of tolerance
What is autoimmunity?

A
  • Failure of various regulatory immune system controls
  • Immune attack of host components
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5
Q

What is tolerance and describe the 2 types?

A
  • Tolerance: Immunosuppression doesn’t attack self proteins or cells
  • Central Tolerance: destroy self-reactive T or B cells before they enter circulation
  • Peripheral Tolerance: destroy or control self reactive T or B cells which enters circulation
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6
Q

Describe central tolerance for B cells?

A
  • Immature B cells in bone marrow -> Encounter antigen in form (stromal cell) which crosslinks their IgM -> Apoptosis triggered
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7
Q

What can be the problem behind selecting T-cell receptors which bind to self MHC?

A
  • Binding is too weak -> signalling may not get activated -> when binding to MHC with foreign peptides
  • Binding is too strong -> signalling occurs -> whether self or foreign peptide
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8
Q

Describe the factors used for T cell selection in the thymus?

A
  • Useless? -> no self-MHC binding -> death by neglet/apoptosis
  • Dangerous? -> binds self MHC too strongly -> apoptosis triggered -> -ve selection
  • Useful? -> binds self MHC weakly -> signal to survive -> + ve selection
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9
Q

How can a T cell developing in the thymus encounter MHC bearing peptides expressed in other parts of the body?

A
  • Specialised TF -> known as Autoimmune regulator (AIRE)
  • Increase self tolerance by allowing thymic expression of genes from other tissues
  • AIRE mutation - autoimmune polyendocrinopathy syndrome type 1 -> multi-organ autoimmunity
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10
Q

Peripheral tolerance
State the mechanisms involved within peripheral tolerance?

A
  • Ignorance
  • Anergy
  • Regulation
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11
Q

Describe the ignorance mechanism involved within peripheral tolerance?

A
  • Includes: antigen present in Decreased concentrations
  • Prevent threshold TCR triggering in immunologically privileged sites (eye, brain)
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12
Q

Describe the anergy mechanism involved within peripheral tolerance?

A
  • Naive T cells require co-stimulatory signals for activation
  • Most cells lack co-s + MHC II
  • If Naive T cell see MHC/peptide ligand without co-s, it becomes anergic -> Decreased stimulation even if co-s is present
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13
Q

Describe the regulation mechanism involved within peripheral tolerance?

A

Treg cells (subset of Th) -> inhibit other T cells via cytokines (IL-10 + TGF-beta) -> defective Treg - multiple sclerosis

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14
Q

Name the Treg expression TF and what its mutation can lead to?

A
  • FOXP3
  • Mutation - severe + fatal autoimmune disorder
  • Immune dysregulation
  • Polyendocrinopathy
  • Enteropathy X-linked (IPEX) syndrome.
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15
Q

Genetic + environmental factors
Describe genetic factors involved within autoimmunity?

A
  • MHC
  • Polymorphism (increased genetic variation) -> associated with disease + autoimmunity
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16
Q

State endocrine factor diseases more common in male than females + vice versa?

A
  • M > F -> Multiple sclerosis, ankylosing spondylitis
  • F > M - SLE
  • F = M -> diabetes
17
Q

Describe hypothesis involved within environmental factors of autoimmunity?

A
  • Hygiene hypothesis -> Non-obese diabetic mice + specific pathogen free
  • Conditions = no diabetes seen -> Migration + T1d, MS + SLE
  • Smoking = rheumatid arthritis
18
Q

Examples of immune mechanisms
Give 4 mechanisms which might trigger a breakdown of self tolerance?

A
  • Loss of/problem with reg. cells
  • Release of sequestered antigen
  • Modification of self
  • Molecular mimicry
19
Q

Describe the modification of self mechanisms stating an example?

A

Citrulline (AA, not via DNA) -> Arginine (+ ve) converted to citrulline (neutral) as post-translational modification by peptidylarginine deiminase (PAD) enzyme + increase via IF -> C residue on peptide = increased degradation chances -> AutoABs to cit. found in RA - clinical diagnosis

20
Q

Describe the molecular mimicry mechanism with an example?

A
  • Diseases triggered via infection with streptococcus pyogenes
  • ABs to stop cell wall antigens cross reacting with cardiac muscle
  • Causes rheumatic fever
21
Q

Describe ABs in autoimmune pathologies outlining 3 examples and describing them?

A
  • Graves disease -> Auto-ABs bind TSHR + stimulate -> hyperthyroidism -> diseases transferred via lqG
  • Myasthenia gravis -> AutoABs bind ACHR -> block ACH binding + receptor internalisation & degradation -> muscle weakness
  • SLE + vasculitis -> AutoABS to soluble antigen -> immune complex formation -> deposited in tissue -> activation of complement + phagocytic cell -> disposition in kidney = renal failure
22
Q

How can newborns suffer from autoimmune diseases?

A
  • Patient transfers anti-Autoimmune infection across placenta into fetus
  • Newborn suffers autoimmune disease
  • Plasmapheresis removes IgG + cures diseases
23
Q

Describe how T cells can be involved in autoimmune pathology?

A
  • T cell destruction -> Direct killing (CD8+), self destruction (cytokines), Macrophages (- tissue destruction), CD4 provide help for AB + cytotoxicity (non-pathogenic IgM -> pathogenic IgG) -> diseases = multiple sclerosis, insulin
24
Q

Describe purpose of TH17 cells and state examples of Autoimmune diseases where they become implicated?

A

Th cells -> produce cytokine IL-17 + highly IF -> immune cells recruitment, migration + activation -> implicated in spondyloarthropathy, MS + diabetes

25
Q

Describe therapeutic strategies used to deal with Al diseases?

A
  • Anti-inflammatories (NSAIDs, corticosteroids)
  • T + B cell depletion (RA: anti-CD4 + CD20-ABs)
  • Therapeutic ABs (anti-T,VLA-4 (blocks adhesion))
  • Antigen specific therapies in development (glatiramer acetate -> Increase T reg

Microbiology And Immunology (32 decks)

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