Type IV hypersensitivity

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Created by:

mebs  on April 12, 2010

Subjects:

Immunology - RUSVM

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Type IV hypersensitivity

Delayed type hypersensitivity, Type IV
T cell mediated hypersensitivity reaction occuring more then 24 hrs after contact with the antigen
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Definitions

Delayed type hypersensitivity, Type IV T cell mediated hypersensitivity reaction occuring more then 24 hrs after contact with the antigen
Delayed type hypersensitivity characeristics an influx of nonspecific inflammatory cells, mostly macrophages into tissues. Lacks antibody involvement
DTH response not always detrimental - but can cause extensive tissue damage and plays an important role in host defense against intracellular pahtogens and contact antigens
causative agents of type IV hypersensitivity rxn bacteria, fungi, protozoa, noninfectious agents (chemicals)
transfer of DTH rxn cannot be transferred via serum, only by T lymphocytes
sensitization phase of DTH 1-2 wks after primary contact with antigen
peptide epitopes and MHC class II proteins, CD4+ T cells associate to result in a ell mediated response and the generation of memory Tdth cells
PPD purified protein derivative, results in activation nof memory Th1 cells by APC and intiation of DTH
activated Tdth cells secrete cytokines that result in vasodilation, increased vascular permeability, and recruitment/activation of macrophages
neutrophil appearence early, 6-12 hrs
blood monocyte and T cell appearence 24-48 hrs after antigen exposure
crucial cytokines TNF-alpha, IFN-y, MCF, MIF, IL-1, TNF-beta
tissue damage in DTH results from release of hydrolytic enzymes and reactive oxygen intermediates from macrophages
the most important clinical form of DTH granulomatous hypersensitivity
granulomas formation due to 1. persistance of particles in macrophage, 2. persistant immune complexes, 3. chronic irritants
ACD allergic contact dermatitis, a T cell mediated eczematous disease
ACD characterized by 48-72 hr delayed eczematous response to the epicutaneous application of the antigen
ACD sensitization phase 10-14 days, haptens form complexes with skin proteins
epidermal langerhans cells modified self proteins in ACD internalized by these cell and then migrate as veiled cell to regional lymph nodes
veiled cells produce in the lumph node present to CD4+ and form memory CD4+ Th1 cells
Tdth Th1 cell
elicitation phase occurs with 48-72 hrs, activation of the Tdth cells and cytokines
CD8+ T cells role contribute to tissue damage by cell-mediated cytotoxicity
lipid soluable chemicals can cross the cell membrane and modify intracellular proteins
lesion acute and chronic eczematous rxn observed in a hairless area
DDX of DTH patch testing, positive test = local erythema and vesiculation
poison ivy exposure oils (urushiol) leads to rash within 12-48hr and persists 2-4wks
pentadecacatechol lipid soluable hapten, formed intermediate of urushiol
poison ivy lesion origin lysis of altered epidermal cells by CD8+ T cells and lytic enzymes released from activated macrophages
treatment for ACD steroids
pathology of ACD mononuclear cell infiltration

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