Linked Life Data

20132230

Source:http://linkedlifedata.com/resource/pubmed/id/20132230

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2010-6-18
pubmed:abstractText
T helper type 1 (Th1)-type polarization plays a critical role in the pathophysiology of acute graft-versus-host disease (aGVHD). The differentiation of T cells into this subtype is dictated by the nature of the donor naive CD4(+) T cell-host antigen presenting cell (APC) interaction. Suppressors of cytokine signalling (SOCS) are a family of molecules that act as negative regulators for cytokine signalling, which regulate the negative cytokine signalling pathway through inhibiting the cytokine-induced Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway. Studies have shown that SOCS proteins are key physiological regulators of both innate and adaptive immunity. These molecules are essential for T cell development and differentiation. SOCS-3 can inhibit polarization to Th1 and contribute to polarization to Th2. In this study, we found that interleukin (IL)-2 pre-incubation of C57BL/6 naive CD4(+) T cells could up-regulate the expression of SOCS-3. Naive CD4(+) T cells constitutively expressed low levels of SOCS-3 mRNA. SOCS-3 mRNA began to rise after 4 h, and reached peak level at 6 h. At 8 h it began to decrease. High expression of SOCS-3 mRNA induced by IL-2 could inhibit the proliferation of naive CD4(+) T cells following stimulation with allogeneic antigen. IL-2-induced high SOCS-3 expression in naive CD4(+) T cells could inhibit polarization to Th1 with stimulation of allogeneic antigens. We have demonstrated that IL-2-induced high SOCS-3 expression in naive CD4(+) T cells could reduce the incidence of aGVHD between major histocompatibility complex (MHC) completely mismatched donor and host when high SOCS3 expression of CD4(+)T cells encounter allogeneic antigen in time. These results show that IL-2-induced high SOCS-3 expression can inhibit aGVHD through inhibiting proliferation and polarization to Th1 with the stimulation of allogeneic antigen.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-10024247, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-10373548, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-10411505, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-10526574, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-11053100, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-11357147, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-11361933, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-11867595, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-11907070, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-12042807, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-12114403, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-12407025, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-12469934, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-12480263, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-12517953, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-12591901, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-12705851, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-12783879, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-12840064, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-12847520, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-12874225, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-12942096, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-12958064, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-12967787, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-1467511, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-14764532, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-15034008, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-15372473, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-15905116, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-16234351, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-17359368, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-17525754, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-17609432, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-2265242, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-3131876, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-7909457, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-8963063, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-9202125, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-9202126, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-9649564, http://linkedlifedata.com/resource/pubmed/commentcorrection/20132230-9886427
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1365-2249
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
160
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
479-88
pubmed:dateRevised
2011-7-28
pubmed:meshHeading
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