Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2008-3-24
pubmed:abstractText
The inducible co-stimulator (ICOS, CD278) is essential to the efficient development of normal and pathological immune reactions. Since ICOS-deficient mice have enhanced susceptibility to experimental allergic encephalomyelitis (EAE), we have functionally analyzed a CD4+ICOS+ population comprising 6-15% of all CD4+ T cells in secondary lymphoid organs of unmanipulated wild-type mice and checked for their ability to suppress EAE. In C57BL/6 mice, CD4+ICOS+ cells were a major source of cytokines including IFN-gamma, IL-2, IL-4, IL-10 or IL-17A. Upon activation, these cells showed preferentially enhanced production of IL-4 or IL-10 but inhibited IFN-gamma production. In contrast, CD4+ICOS- cells mainly produced IFN-gamma. Interestingly, CD4+ICOS+ cells partially suppressed the proliferation of CD4+ICOS- or CD4+CD25- lymphocytes 'in vitro' by an IL-10-dependent mechanism. Furthermore, CD4+ICOS+ activated and expanded under appropriate conditions yielded a population enriched in cells producing IL-10 and T(h)2 cytokines that also suppressed the proliferation of CD4+CD25- lymphocytes. CD4+ICOS+ cells, before or after expansion in vitro, reduced the severity of EAE when transferred to ICOS-deficient mice. In the same EAE model, lymph node cells from ICOS-deficient mice receiving ICOS+ cells showed reduced IL-17A production and enhanced IL-10 secretion upon antigen activation in vitro. Thus, naturally occurring CD4+ICOS+ cells, expanded or not in vitro, are functionally relevant cells able of protecting ICOS-deficient mice from severe EAE.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1460-2377
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
577-89
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:18310064-Adoptive Transfer, pubmed-meshheading:18310064-Animals, pubmed-meshheading:18310064-Antigens, Differentiation, T-Lymphocyte, pubmed-meshheading:18310064-CD4-Positive T-Lymphocytes, pubmed-meshheading:18310064-Cell Proliferation, pubmed-meshheading:18310064-Cells, Cultured, pubmed-meshheading:18310064-Disease Models, Animal, pubmed-meshheading:18310064-Encephalomyelitis, Autoimmune, Experimental, pubmed-meshheading:18310064-Inducible T-Cell Co-Stimulator Protein, pubmed-meshheading:18310064-Interleukin-10, pubmed-meshheading:18310064-Interleukin-17, pubmed-meshheading:18310064-Lymphocyte Activation, pubmed-meshheading:18310064-Mice, pubmed-meshheading:18310064-Mice, Inbred BALB C, pubmed-meshheading:18310064-Mice, Inbred C57BL, pubmed-meshheading:18310064-Mice, Knockout, pubmed-meshheading:18310064-T-Lymphocytes, Regulatory, pubmed-meshheading:18310064-Th2 Cells
pubmed:year
2008
pubmed:articleTitle
CD4+ICOS+ T lymphocytes inhibit T cell activation 'in vitro' and attenuate autoimmune encephalitis 'in vivo'.
pubmed:affiliation
Departamento de Inmunología, Centro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas, Ramiro de Maeztu 9, E-28040 Madrid, Spain. jmrojo@cib.csic.es
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't