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Immunology II > Autoimmunity > Flashcards

Autoimmunity Flashcards

1
Q

Describe Central and Peripheral tolerance

A

Central: Autoreactive lymphocytes not deleted in bone marrow and thymus

Peripheral: Normal inhibitory mechanisms fail in the periphery.

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2
Q

What are some pre-disoposing factors of autoimmunity

A

Factors influencing development

  • ->Abnormalities of lymphocytes and APC’s
  • -> Genetic predisposition
  • -> Microbial infections

Tissue injury can be brought about by:

  • -> autoreactive CTL’s
  • -> Circulating autoantibodies
  • -> immune complexes
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3
Q

Define Vertical transmission of antibodies

A

Maternal autoimmune IgG may affect developing fetus/neonate

  • -> effects disappear after birth when antibodies are catabolized
  • -> some organ damage may be irreversible, e.g. developing heart is damaged by autoantibodies.
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4
Q

Define Autoimmune Hemolytic anemia (organ specific)

A
  • -> RBC antibodies produced against RBC membrane proteins
  • -> causes RBC lysis and anemia
  • -> opsonization –> removal by phagocytic cells in spleen
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5
Q

Goodpasture syndrome (organ specific)

A
  • -> Autoantibodies to the alpha3 chain of type IV collage (basement membrane collage) of the lung (alveoli) and the kidney (glomeruli)
  • -> causes complement activation –> kidney damage, pulmonary hemorrhage, death (within few months)
  • -> Smooth, ribbon like appearance
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6
Q

Pernicious anemia (organ specific)

A
  • -> Autoantibodies to intrinsic factor and or gastric parietal cells
  • -> decreased absorption of vitamin B12 –> abnormal erythropoiesis/anemia
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7
Q

Hasimotos thyroiditis (organ specific)

A
  • -> Hypothyroid state

- -> Autoantibodies and autoreactive T cells to thyroid gland proteins

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8
Q

Idiopathic thrombocytopenia purpura (ITP) (organ specific)

A
  • -> platelets destroyed by autoantibodies to platelet membrane proteins
  • -> “purpura” = purple skin lesions due to epidermal hemorrhage
  • -> IVIG can prevent destruction of platelets
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9
Q

Vitiligo (organ specific)

A

depigmentation of skin by destruction of melanocytes

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10
Q

Graves Disease (organ specific(

A
  • -> autoantibodies against TSH receptor

- -> causes hyperthyroidism

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11
Q

Myasthenia gravis (organ specifc)

A
  • -> autoantibodies to alpha chain of nicotinic acetylcholine receptor on skeletal muscle cells at neuromuscular junctions
  • -> blockage of neuromuscular transmission leads to muscle weakness and paralysis
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12
Q

Type 1A diabetes (organ specific)

A
  • -> Autoantibodies to beta-cells. Despite diagnostic worth of antibodies, autoreactive T cells mediate destruction of beta-cells
  • -> damage to beta cells result in decrease in insulin and increase in blood glucose levels
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13
Q

Multiple Sclerosis (organ specific)

A

Autoimmune demyelinating disease of CNS

  • -> TH1 and TH17 cells specific for myelin antigens become activated, which drives macrophage activation and subsequent damage to myelin-containing nerve cells
  • -> Therapies = interferon and steroid injections
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14
Q

Systemic Lupus erythematosus (systemic)

A
  • -> Broad loss of regulatory control that sustains self-tolerance
  • -> Autoantibodies against numerous antigens including DNA, RNA, proteins and ribonucleoproteins
  • -> most organ systems can be affected (skin, joints, kidney more frequently)
  • -> more common in females than males
  • -> Most tissue injury mediated by immune complex (TYPE III autoimmunity)
  • -> principal danger = kidney failure due to the passage of immune complexes through the glomerulus and deposition on renal podocytes (express CR1 protein that binds C3b on the immune complex which initiates damage)
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15
Q

Describe the predisposition of Sytemic lupus erythematosus

A
    • Genetic factors involved –> family members have increase incidence of SLE
    • Non genetic factors –> drugs and some viruses (reverses upon removal of drug
    • Immunologic factors –> B cell hyperactivity, increased T-helper activity and or decrease Treg activity
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16
Q

Define Rheumatoid arthritis (RA) (systemic)

A

Progressive inflammatory disease of joints –> destruction of joint cartilage and inflammation of synovium:
–> association of RA with HLA-DR4 haplotype

  • -> TH1 and TH17 macrophages, B cells and plasma cells creat an inflammatory enviornement consisting of secretion of leukocyte-recruiting cytokines
  • -> rheumatoid factor –> IgM/IgG to Fc portion of IgG leads to immune complex
17
Q

Sjogren’s syndrome (systemic

A

Dry eyes + dry mouth caused by destruction of lacrimal and salivary glands:

  • ->B and T cell influx into glands, but not known whether CMI or humoral immunity responsible for damage
  • -> occurs alone or in conjunction with RA or SLE
18
Q

Scleroderma (progressive systemic sclerosis (systemic))

A

Excessive deposition of collagen –> skin, kidneys, GI tract, heart, muscles, lungs:
–> T cells infiltrate dermis –> may have a hypersensitivity to collagen that results in release of Il-1 and TNF-alpha which causes production of collagen and propagates the vicious cycle

19
Q

Polymyositis-dermatomyositis (systemic)

A

Polymyositis = muscle injury possibly brought about by CD4+ and CD8+ T lymphocytes infiltration of muscles
Dermatomyositis = skin rash that often accompanies polymyositis
–> 25% have autoantibodies to histidyl t RNA synthetase (diagnostic)
–> coxsackie B viruses could play a role as it has been isolated from some patients

20
Q

Describe nonspecific immunosuprressent autoimmune treatment options

A

Corticosteroids: Prednisone = anti-inflammatory effects

Azathioprine and cyclophosphamide: Cytotoxic drugs that interfere with DNA synthesis –> eliminates dividing lymphocytes

Cyclosporine and tacrolimus: Block activity of calcineurin –> blocks transcription of IL-2 etc.

Plasmapheresis: removes Ag-Ab complexes –> short-term alleviation of symptoms

21
Q

Describe Antagonism of TNF-alpha treatments

A

Antagonism of TNF-alpha relive the symptomes of some diseases:

  • Infliximab = humanized anti-TNF-alpha monoclonal antibody
  • Etanercept = soluble TNF-alpha receptor fusion protein that binds TNF-alpha
  • Adalimumab = recominant human IgG1 monoclonal

Very potent anti-inflammatories that may be used to treat crohn’s disease, rheumatoid arthritis, juvenile chronic arthritis and ankylosing spondylitis

Immunology II (8 decks)

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