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1996-02-27
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Document 0728
DOCN M9630728
TI Alpha-melanocyte-stimulating hormone suppresses antigen-stimulated T
cell production of gamma-interferon.
DT 9603
AU Taylor AW; Streilein JW; Cousins SW; Schepens Eye Research Institute,
Boston, MA 02114, USA.
SO Neuroimmunomodulation. 1994 May-Jun;1(3):188-94. Unique Identifier :
AIDSLINE MED/96053032
AB The neuropeptide alpha-melanocyte-stimulating hormone (alpha-MSH) is
known to suppress cytokine-mediated inflammation. In addition, we
previously found that alpha-MSH suppressed the production of the
proinflammatory cytokine interferon (IFN)-gamma by antigen-stimulated
primed lymph node T cells. This immunosuppressive activity of alpha-MSH
on lymph node T cell cultures is similar to that of interleukin (IL)-4.
To further examine the potential 'IL-4 like' activities of alpha-MSH,
antigen-stimulated lymph node T cell cultures were treated with
alpha-MSH in the presence of neutralizing anti-IL-4 antibodies. The
enhanced production of IFN-gamma caused by the presence of anti-IL-4
alone in the T cell cultures was squelched by alpha-MSH. This
demonstrated that in these cultures, alpha-MSH regulation of IFN-gamma
production operates in a fashion similar to that of endogenous IL-4.
Addition of exogenous IL-4 to antigen-stimulated lymph node T cell
cultures did not intensify alpha-MSH down-regulation of IFN-gamma
production, and the addition of alpha-MSH to IL-4-treated cultures did
not further depress IFN-gamma production. These and the previous results
suggest that the mechanism of alpha-MSH suppression of IFN-gamma
production in the antigen-stimulated T cell cultures is similar to, but
independent of, IL-4. When antigen-presenting cells (APCs) were the only
cells in the antigen-stimulated T cell cultures treated with alpha-MSH,
there was a significant reduction (60-70%) of APC elicitation of
IFN-gamma production by untreated primed T cells.(ABSTRACT TRUNCATED AT
250 WORDS)
DE alpha-MSH/*PHARMACOLOGY Animal Antigen Presentation/*DRUG EFFECTS
Antigens, Bacterial/IMMUNOLOGY Depression, Chemical
Inflammation/PHYSIOPATHOLOGY Interferon Type II/*BIOSYNTHESIS/GENETICS
Lymph Nodes/CYTOLOGY Lymphocyte Transformation Mice Mice, Inbred BALB
C Mycobacterium tuberculosis/IMMUNOLOGY
Neuroimmunomodulation/*PHYSIOLOGY Support, U.S. Gov't, P.H.S. Th1
Cells/*DRUG EFFECTS/IMMUNOLOGY/METABOLISM JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).