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31 Cards in this Set

  • Front
  • Back
What are two main types of type IV hypersensitivity?
-delayed type hypersensitivity
-t-cell mediated hypersensitivity
Do the type IV type hypersensitivity reactions involve antibodies?
NO
What is the cause of cell/tissue injury in type IV?
cell-mediated immune response with sensitized T lymphocytes
Describe the mechanism of a delayed type 4 hypersensitivity reaction?
-APC presenting cell releases IL12 and activates Th1 CD4 which secretes three types of cytokiens
-APC also releases IL21, that activates TH17 --> recruits neutrophils
Describe the mechanism of a T-cell mediated hypersensitivity reaction:
CD8 directly kill cells
What are the two prototypes of DTH?
-Tuberculosis and contact dermatitis
Describe the host response to a tubercolosis infection.
-first exposure of mycobacterium tuberculosis: macrophages engulf mycobacteria but no succeed in eliminating
-MHC2 and release of IL12
-Th cell activate and release IL2, TNF, IFN-gamma
Three major cytokines produced by TH1 and functions?
IFN: activate macrophages
TNF: leakky cells
IL-2 activate itself / more TH1
With persistent AG like Myc tuberc, when is the initial perivascular lymphocytic infiltrate replaced by macrophages?
2-3 weeks
define a granuloma:
epitheloid cells (morphologically transformed macrophages) surrounded by rim of lymphocytes also containing giant cells
What is this?
What is this?
Lymph node with several granulomas
how many weeks does it take to battle mycobacterium? how many weeks does it take to recruit macrophages and form granuloma/
3 weeks and 3 weeks
What does PPD stand for? What is another name for it -when does induration begin? when does the reaction peak?
-protein positive derivative or Mantoux
-begins 8-12 hours
-peaks at 24-72 hours
Give two cellular explanations to explain what is going on in a positive TB test:
1.) accumulation of mononuclear cells around small veins (perivascular cuffing)
2.) increased microvascular permeability --> escape of plasma proteins (dermal edema and deposition of fibrin)
what is perivascular cuffing?
-accumulation of mononuclear cells (T lymphs CD4) around small veins and venules
What is this?
What is this?
immunoperoxidase staining showing perivascular cuffing
Why is the PPD test sometimes given as a two-step PPD?
-elderly person had exposure in the past and has waning reaction so negative TB test at first
-a repeat PPD 1-3 weeks after may result in a boosted reaction
how many weeks later do you give the second PPD in a two step PPD?
1-3 weeks after first
What is contact dermatitis an example of?
type 4 delayed type hypersensitivity
What are haptens and give exampls of haptens
a hapten is a small molecule that can elicit an immune response only when attached to a large carrier such as a protein

1.) resins in poison ivy and oak
2.) metals such as nickel
3.) acetylates and chemicals in rubber
-what is the antigen in poison ivy (also a type of hapten)
urshiol or catechol molecule
Why does no dermatitis result from primary contact?
-catechols are catabolized before sensitized T cells are produced (7-10 days produce memory cells though)
what happens during secondary contact with poison ivy? (explain the histopathology of this slide)
what happens during secondary contact with poison ivy? (explain the histopathology of this slide)
in 1-2 days, get dermatitis: Th1 cells accumulate and release cytokines that cause damage to keratinocytes; cause separation of these cells
T-cell mediated cytotoxicity plays a role in 4 different categories. list categories
-resistance to viral infections (hep b)
-tumor immunity
-autoimmune diseases
-graft versus host ; graft rejection
What is this and what accounts for the damage?
What is this and what accounts for the damage?
liver injury; HBV virus
-host immune response to viral AGs on infected hepatocytes leads to T-cell mediated cytotoxicity and tissue damage:
Explain the role of type 4 sensitivity in type 1 diabetes. What is unique about this?
-both types of type 4: DTH and CT-mediated
-failure of self-tolerance in T cells
-Damage to beta cells:
1.) Th1 cells by secreting IFN-gamma and TNF
2.) CD8 cells by directly killing Beta cells
explain role of Type IV in MS. Is it mainly DTH or cytotoxic T-cell mediated type?
-mainly DTH
-TH1 and Th17 react against myelin antigens and secrete cytokines
-Th1: IFN-gamma
-Th17: recruitement of leukocytes
evidence for TYPE IV in guillain bare and examples of preceding infections
evidence:
1.) transfer of T cells to animals: comparable lesions
2.) lymphocytes from individuals with GB: demyelination in tissue cultures of myelinated nerves

preceding infections: influenza, campylobacter jejuni, CMV, EBV
Graft versus host and Host versus graft plays role in T cell cytotoxicity? Where do we see GVH?
yes
-GVH in bone marrow transplants typically
What are two mechanisms in T-cell mediated cytotoxicity?
FAS-FAS ligand and perforin/granyzme
explain the complications of hashimoto thyroiditis? What types of hypersensitivity reactions are involved? (there are 3)
-T-cell mediated cytotoxicity (fas-fass with CD*)
-thyrocyte injury (TH1 CD4 with IFN-gamma)
-antibody dependent cell mediated cytotoxicity with N cells