Immune Mediated Tissue Damage Flashcards

1
Q

Can Th2 cells induce type IV hypersens?

A

No only Th1 and Th17 can.

-Th2 cells induce lesions that are part of immediate hypersens. (Type I) and are not conisdered a form of type IV.

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2
Q

Is immediete-type hypersen monoclonal or polyclonal?

A

Polyclonal with more then just 1 B-cell involved and more then one IgE.

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3
Q

What does degranulation of mast cells release?

A

Histamine, proteases, and chemotactic factors

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4
Q

What cytokines are important for type I hypersen.?

A

IL-1, IL-2, IL3, IL-4, IL-5, IL-6

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5
Q

What are the important arachidonic acid metabolite produced in type I hypersens.?

A

PLA2 produces prostagladins and Leukotriene B4, C4, and D4, as well as PAF

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6
Q

What is this and what is it caused by?

A

This is a type I hypersen to asthma.

-it is chronic inflammation that is causing tissue remodeling, mucsou production blockings airways, and bronchoconstriction

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7
Q

What is going on here?

A

This is asthma again a type I hypersen.

It is a high power of the previous picture with eosinophils and mononuclear cells present. The chronic inflammatory cells are known to cause irreversible, although mild, lung injury (interstitial fibrosis and remodeling) in astham, so it is imperative that asthma be well controlled to avoid chronic lung problems later in life.

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8
Q

What is the casue of autoimmune hemolytic anemia?

A

Individuals produce auto antibodies to their own blood cells which causes them to be destroyed. This is an example of a type II hypersens.

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9
Q

What is the cause of Goodpasture’s Syndrome?

A

Autoantibodies to the non-collagenous protein in basement membranes of kidney glomeruli and lung alveoli leading to complement and Fc-receptor mediated inflammation.

-leads to Nephritis and or lung hemorrhages

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10
Q

What is this?

A

Linear basement membrane fluorescene in Goodpasture syndrome, casued by an IgG or IgM antibody against collagen type IV, which is of course in basement membranes

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11
Q

What is the cause of polyarteritis nodosa?

A

Antigens to Hep B virus resulting in systemic vasculitis

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12
Q

Explain the mechanism of type III hypersen.?

A

Antibodes-antigen immune complexes of IgG or IgM are deposited in tissue, which activate complement and other factors of inflammation. Most often affected are the skin, and the kidneys (glomerulus), also in the joints as arthritis

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13
Q

What is this?

A

Post Steptococcal glomerulonephritis. Note the hypercellular glomerulus. Many of the extra nuclei are PMNs, attracted by chemokines, and attached to the membrane via C3b and Fc receptors.

  • example of type III hypersens.
  • too many neutrophils leads to scarring and renal failure
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14
Q

In type III hypersens, what immune complex size is most dangerous?

A

Immune complexes of ideal size are formed with slight antigen excess.

  • too large of complexes are removed by mononuclear phagocyte systems
  • compllexes likely induce disease by attaching to Fc or C3b receptors on neutrophils, and trigger release of cytokines, attracting more PMNs, and initiating more complement fixation.
  • see clinically as decrased serum levels of C3 due to their consumption by the immune complexes
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15
Q

What is a Langhans giant cell?

A

formation of macrophages during inflammation, (seen in type IV hypersen).

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16
Q

What are the two different pathogenesis for tissue damage in type IV hypersen.?

A

through cytokine-mediated inflammation by CD4 cells

or

by T-cell mediated cytolysis by CD8 cells.

17
Q

Describe what is going on here

A

This is granulomatous inflammation in type IV reaction.

-

18
Q

What is this?

A

This is a non-caseating granuloma

19
Q

What is this an image of?

A

Caseating Granuloma in pulmonary tuberculosis, widely considered to be a type IV hypersensitivity disease. This is because Mycobacterium Tuberculosis has no toxins, and usually very few organisms can be found, often located in epithelioid histocytes or Langhans giant cells.

-After 2 to 3 weeks of sustained activation macrophages often undergo a morphologic transformation into epithelioid cells, which are large-epithelium like cells with abundant pink cytoplasm. Usually associated with strong Th1-cell activation and lots of IFN-gamma

20
Q

What is this

A

A DTH in the skin. You see perivascular accumulation (cuffing) of mononuclear inflammatory cells (lymphocytes and macrophages), with associated dermal edema and fibrin deposition. In B, you have immunoperoxidase staining revelas a predominantly perivascular cellular infiltrate that marks positvely with anti-CD4 antibodies