Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2001-5-21
pubmed:abstractText
Several studies have provided indirect evidence in support of a role for beta cell-specific Th2 cells in regulating insulin-dependent diabetes (IDDM). Whether a homogeneous population of Th2 cells having a defined beta cell Ag specificity can prevent or suppress autoimmune diabetes is still unclear. In fact, recent studies have demonstrated that beta cell-specific Th2 cell clones can induce IDDM. In this study we have established Th cell clones specific for glutamic acid decarboxylase 65 (GAD65), a known beta cell autoantigen, from young unimmunized nonobese diabetic (NOD) mice. Adoptive transfer of a GAD65-specific Th2 cell clone (characterized by the secretion of IL-4, IL-5, and IL-10, but not IFN-gamma or TGF-beta) into 2- or 12-wk-old NOD female recipients prevented the progression of insulitis and subsequent development of overt IDDM. This prevention was marked by the establishment of a Th2-like cytokine profile in response to a panel of beta cell autoantigens in cultures established from the spleen and pancreatic lymph nodes of recipient mice. The immunoregulatory function of a given Th cell clone was dependent on the relative levels of IFN-gamma vs IL-4 and IL-10 secreted. These results provide direct evidence that beta cell-specific Th2 cells can indeed prevent and suppress autoimmune diabetes in NOD mice.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
166
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6925-36
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11359854-Adoptive Transfer, pubmed-meshheading:11359854-Age of Onset, pubmed-meshheading:11359854-Animals, pubmed-meshheading:11359854-Cell Culture Techniques, pubmed-meshheading:11359854-Cell Movement, pubmed-meshheading:11359854-Clone Cells, pubmed-meshheading:11359854-Cytokines, pubmed-meshheading:11359854-Diabetes Mellitus, Type 1, pubmed-meshheading:11359854-Epitopes, T-Lymphocyte, pubmed-meshheading:11359854-Female, pubmed-meshheading:11359854-Glutamate Decarboxylase, pubmed-meshheading:11359854-Interleukin-4, pubmed-meshheading:11359854-Islets of Langerhans, pubmed-meshheading:11359854-Isoenzymes, pubmed-meshheading:11359854-Mice, pubmed-meshheading:11359854-Mice, Inbred NOD, pubmed-meshheading:11359854-Mice, SCID, pubmed-meshheading:11359854-Spleen, pubmed-meshheading:11359854-T-Lymphocyte Subsets, pubmed-meshheading:11359854-T-Lymphocytes, Helper-Inducer, pubmed-meshheading:11359854-Th2 Cells
pubmed:year
2001
pubmed:articleTitle
A glutamic acid decarboxylase 65-specific Th2 cell clone immunoregulates autoimmune diabetes in nonobese diabetic mice.
pubmed:affiliation
Department of Microbiology and Immunology, Mary Ellen Jones Building, Room 804, Campus Box 7290, University of North Carolina, Chapel Hill, NC 27599-7290, USA. mtisch@med.unc.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.