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Immunology > Lecture 12: Autoimmunity > Flashcards

Lecture 12: Autoimmunity Flashcards

1
Q

What is Koch’s postulates?

A
  1. Isolate the pathogen (Virus, microbe,etc) from sick creature 2. Grow the pathogen in the laboratory and obtain a pure culture 3. Inoculate a healthy creature with a sample from pure culture. The pathogen should cause the same disease symptoms that were seen in first creature 4. Re-isolate the same pathogen from second sick animal
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2
Q

Autoimmune disease

A

Clinical manifestation directly linked to immune cell activation Evidence of T and or B cell autoimmunity Disease is transferred in animal models by adoptive transfer of T cells or autoantibodies or immunisation with self-Antigens Exclusion of an infective cause Often familiarity or “clustering” of AD Genetic predisposition and environmental trigger

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3
Q

What type are related to autoimmune diseases?

A

Type II, III, IV diseases

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4
Q

What is type I hypersensitivity reactions related to?

A

Allergy

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5
Q

What is type 1 classification ?

A

Binding of Ig to Fc receptor which activated mast cell and basophils There is a burst of granules and this gives you fever/ asthma attack

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6
Q

What is type 2 classification?

A

Conduction of Antibodies which are directly pathogenic Binds to either receptor or particular cell type Cause damage by: ADDC or complement activation

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7
Q

What is type 3 classification?

A

Stimulated by antibodies Immune complexes Once the complexes are deposited in the kidney of glomerulus - activate complement that attract cells of immune system

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8
Q

What is type 4 classification?

A

Delayed hypersensitivity reactions Involved in organic specific chronic inflammatory diseases Involved in intracellular pathogens

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9
Q

Give examples of Type I reactions

A

Churg-Strauss Vasculitis Eosinophilic diseases

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10
Q

Give examples of type II Hypersensitivity reactions

A

Hemolytic anemia, Myasthenia Agra is, Graves’ disease, SLE

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11
Q

Give examples of type III hypersensitivity reactions

A

SLE, Panarteritis Nodosa, RA

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12
Q

Give examples of IV hypersensitivity reactions

A

Crohn’s disease, Rheumatoid arthritis

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13
Q

What are the FC Gamma receptors?

A

2B1 and 2B2 are non-inhibitory Fc receptors

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14
Q

What does Fc Gamma III do?

A

Kill tumour cells

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15
Q

What are the cell types of FcyR1?

A

Macrophages, neutrophils, Eosinophils, Dendritic cells

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16
Q

What is the effect of ligation for FcyRI?

A

Uptake, respiratory burst

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17
Q

What is the cell type got FcyRIIA?

A

Macrophages, neutrophils, eosinophils, platelets, Langerhan cells

18
Q

What is the effect of ligation for FcyRIIA?

A

Uptake, granule release

19
Q

What is the cell type for FcyRIIB1?

A

B cells, mast cells

20
Q

What is the effect of ligation for FcyRIIB1?

A

No uptake, inhibition of stimulation

21
Q

What is the cell type got FcyRIIB2?

A

Macrophages, Neutrophils, Eosinophils

22
Q

What is the effect of ligation for FcyRIIB2?

A

Uptake, inhibition of stimulation

23
Q

What is the cell type of FcyRIII?

A

NK cells, Eosinophils, macrophages, neutrophils, mast cells

24
Q

What is the process of ADDC?

A

Antibodies bind antigens on the surface of target cells NK Cell CD16 Fc receptors recognise cell- bound antibodies Cross-linking of CD16 triggers degranulation into lytic synapse Target Cell die by apoptosis

25
Q

What is goodpasture glomerulonephritis?

A

Rare autoimmune disease in which antibodies attack the basement membrane in lungs and kidneys - bleeding from lungs and kidney failure

26
Q

What is SLE glomerulonephritis?

A

Inflammation of kidneys caused by systemic lupus erythematosus Auto-Immune disease - glomeruli become inflamed

27
Q

What is Rheumatoid Arthritis?

A

Chronic inflammatory destructive arthropathy

28
Q

What is the pathogenesis of Rheumatoid Arthritis ?

A

Inflamed of synovial membrane

29
Q

What is the evidence of RA as autoimmune disease?

A

B cell compartment: Autoantibodies. Rheumatoid factor (IgM anti-IgG) Anti-citrullinated proteins (ACPA). Collagen, BiP, RA33. T cell compartment: HLA-DRQ (shared epitope)

30
Q

What is the Role of M1?

A

TH1, tumour Resistance, Killing of intracellular parasites, tissue destruction

31
Q

What is the role of M2s?

A

Parasite encapsulation, immunoregulation, Angiogenesis, tissue remodelling, tumour promotion time

32
Q

What is M1 activated by?

A

Classical activation: IFNgamma, LPS, TNFalpha

33
Q

What is activated by M2?

A

Alternative activation: Il-4, IL-13, IL-10, TGF beta

34
Q

What does M1 cause?

A

Cytotoxicity tissue injury

35
Q

What does M2 lead to?

A

Immune suppression: tissue repair

36
Q

TNF- alpha

A

Proinflammatory cytokine release: IL-1, IL-6, IL-23 and GM-CSF

37
Q

TNF alpha

A

Hepcidin induction: acute-phase response PGE2 Production Osteoblasts Activation (bone resorption) Chondrocyte Activation (metalloproteinaise production, cartilage destruction) Angiogenesis Leukocyte accumulation ( induction/ maintenance of HLA class II Expression) Endothelial Cell Activation (upregulation of E-selectin and VCAm-1, leukocyte accumulation) Chemokines release (RANTES, MCP-1, IL-8 and SDF-1) - leukocyte accumulation

38
Q

IL-2, IFN-Gamma, TNF-alpha

A

Cell mediated immunity
Intracellular pathogens
Immunopathology
Organ-specific autoimmunity

39
Q

IL-17

A

Gut bacteria

Immunopathology Arthritis

40
Q

TH2: IL4, IL5, IL10, IL-13

A

Helminths humoral immunity
Immunopathology
Allergy
Atopyy

Immunology (20 decks)

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