home
***
CD-ROM
|
disk
|
FTP
|
other
***
search
/
Collection of Education
/
collectionofeducationcarat1997.iso
/
HEALTH
/
MED9601.ZIP
/
M9610401.TXT
< prev
next >
Wrap
Text File
|
1996-01-30
|
3KB
|
46 lines
Document 0401
DOCN M9610401
TI Self-antigen-induced Th2 responses in experimental allergic
encephalomyelitis (EAE)-resistant mice. Th2-mediated suppression of
autoimmune disease.
DT 9601
AU Cua DJ; Hinton DR; Stohlman SA; Department of Molecular Microbiology and
Immunology, University; of Southern California School of Medicine, Los
Angeles 90033,; USA.
SO J Immunol. 1995 Oct 15;155(8):4052-9. Unique Identifier : AIDSLINE
MED/96003449
AB Immunization of a limited number of rodent strains with central nervous
system-derived Ags induces experimental allergic encephalomyelitis
(EAE). In contrast to susceptible female SJL mice, age-matched males are
resistant to actively induced EAE. The ability of immunization with
neuroAg to induce Ag-specific T cell activation in resistant male mice
was examined. Ag-specific T cell proliferation was found following
immunization of both male and female SJL mice. Draining lymph node
cytokine mRNA patterns demonstrated that immunization of EAE-resistant
male mice resulted in a Th2-type pattern. By contrast, immunization of
EAE-susceptible female mice resulted in a Th1-type pattern. Priming of
Th1- and Th2-type responses was confirmed by analysis of cytokines
secreted following Ag-specific proliferation. In contrast to the
transfer of myelin basic protein (MBP)-specific Th1-type T cells derived
from female mice, which induced acute and relapse EAE, transfer of
MBP-specific Th2-type T cells derived from male mice resulted in no
clinical or histologic evidence of EAE. A mixture of MBP-specific Th1
and Th2 type cells was transferred to naive recipients to determine if
the neuroAg-specific Th2-type cells exerted a regulatory influence on
EAE. Acute disease was partially eliminated and relapses were completely
eliminated in these recipients. Analysis of spinal cords showed the
presence of both Th1 and Th2 cytokine mRNAs. These data are consistent
with both the ability of Th2-type cells to suppress autoimmunity and a
homeostatic mechanism of T cell regulation based on the cross-regulation
of Th1 and Th2 cells in the maintenance of peripheral tolerance.
DE Animal Autoantigens/*IMMUNOLOGY Disease Susceptibility
Encephalomyelitis, Allergic/ETIOLOGY/*IMMUNOLOGY/THERAPY Female
Immunity, Natural Immunotherapy, Adoptive *Lymphocyte Transformation
Male Mice Mice, Inbred Strains Myelin Basic Proteins/IMMUNOLOGY Self
Tolerance Support, Non-U.S. Gov't Th2 Cells/*IMMUNOLOGY JOURNAL
ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).