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M9550137.TXT
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1995-03-04
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Document 0137
DOCN M9550137
TI The role of TNF-alpha in T-cell-mediated inflammation depends on the
Th1/Th2 cytokine balance.
DT 9505
AU Hernandez-Pando R; Rook GA; Department of Pathology, Instituto Nacional
de la Nutricion; Salvador Zubiran, Mexico DF.
SO Immunology. 1994 Aug;82(4):591-5. Unique Identifier : AIDSLINE
MED/95137621
AB The role of tumour necrosis factor-alpha (TNF-alpha) in tuberculosis is
paradoxical because although there is much evidence for a protective
role, there is also evidence that it plays a part in the tissue damage
that characterizes human disease. We have shown previously that
TNF-alpha frequently induces necrosis when injected into sites
undergoing delayed-type hypersensitivity (DTH) responses to
mycobacterial antigen. This is dependent on CD4+ T cells. However the
presence of this sensitivity to TNF-alpha-induced necrosis depended on
the immunization protocol. We have tested the hypothesis that
sensitivity to TNF-alpha depends on the cytokine profile of the induced
T-cell response. All subcutaneous doses of mycobacterial immunogen used
(10(7) to 10(9) organisms) primed spleen cells so that they secreted
interferon-gamma (IFN-gamma) and interleukin-2 (IL-2) when cultured in
vitro with soluble antigen. However priming for production of IL-4 was
dose dependent as in other systems, and was produced at all times from 7
to 30 days after immunization with 10(9) organisms. Time-course studies
over 30 days showed that sensitivity to TNF-alpha was found in DTH sites
of animals primed for IL-4 and IFN-gamma production, but not in animals
primed only for the Th1 cytokines. We suggest therefore that the
paradoxical role of TNF-alpha can be resolved. In 'pure' Th1 responses
it may act as an additional macrophage-activating factor. In mixed Th1 +
Th2 or Th0 responses it may cause tissue damage. This mixed pattern is
characteristic of tuberculosis, and of the late stage of many chronic
infections where elimination of the infecting organism is failing, and
chronic tissue damage is seen.
DE Animal Antigens, Bacterial/ADMINISTRATION & DOSAGE/*IMMUNOLOGY
Cytokines/*BIOSYNTHESIS Dose-Response Relationship, Immunologic
Hypersensitivity, Delayed/IMMUNOLOGY Immunization/METHODS Interferon
Type II/BIOSYNTHESIS Interleukin-4/BIOSYNTHESIS Kinetics Mice Mice,
Inbred C57BL Mycobacterium/*IMMUNOLOGY Recombinant Proteins/IMMUNOLOGY
Support, Non-U.S. Gov't T-Lymphocytes, Helper-Inducer/*IMMUNOLOGY Th1
Cells/IMMUNOLOGY Th2 Cells/IMMUNOLOGY Tumor Necrosis
Factor/*IMMUNOLOGY JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).