Source:http://linkedlifedata.com/resource/pubmed/id/21841129
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
6
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| pubmed:dateCreated |
2011-9-8
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| pubmed:abstractText |
The T cell-dependent B cell response relies on cognate interaction between B cells and CD4(+) Th cells. However, the consequences of this interaction for CD4(+) T cells are not entirely known. B cells generally promote CD4(+) T cell responses to pathogens, albeit to a variable degree. In contrast, CD4(+) T cell responses to self- or tumor Ags are often suppressed by B cells. In this study, we demonstrated that interaction with B cells dramatically inhibited the function of virus-specific CD4(+) T cells in retroviral infection. We have used Friend virus infection of mice as a model for retroviral infection, in which the behavior of virus-specific CD4(+) T cells was monitored according to their TCR avidity. We report that avidity for Ag and interaction with B cells determine distinct aspects of the primary CD4(+) T cell response to Friend virus infection. Virus-specific CD4(+) T cells followed exclusive Th1 and T follicular helper (Tfh) differentiation. High avidity for Ag facilitated expansion during priming and enhanced the capacity for IFN-? and IL-21 production. In contrast, Tfh differentiation was not affected by avidity for Ag. By reducing or preventing B cell interaction, we found that B cells promoted Tfh differentiation, induced programmed death 1 expression, and inhibited IFN-? production by virus-specific CD4(+) T cells. Ultimately, B cells protected hosts from CD4(+) T cell-mediated immune pathology, at the detriment of CD4(+) T cell-mediated protective immunity. Our results suggest that B cell presentation of vaccine Ags could be manipulated to direct the appropriate CD4(+) T cell response.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Sep
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| pubmed:issn |
1550-6606
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:day |
15
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| pubmed:volume |
187
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
3321-30
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| pubmed:meshHeading |
pubmed-meshheading:21841129-Adoptive Transfer,
pubmed-meshheading:21841129-Animals,
pubmed-meshheading:21841129-Antigen Presentation,
pubmed-meshheading:21841129-B-Lymphocytes,
pubmed-meshheading:21841129-CD4-Positive T-Lymphocytes,
pubmed-meshheading:21841129-Cell Differentiation,
pubmed-meshheading:21841129-Cell Separation,
pubmed-meshheading:21841129-Flow Cytometry,
pubmed-meshheading:21841129-Friend murine leukemia virus,
pubmed-meshheading:21841129-Gene Expression Profiling,
pubmed-meshheading:21841129-Lymphocyte Activation,
pubmed-meshheading:21841129-Mice,
pubmed-meshheading:21841129-Mice, Inbred C57BL,
pubmed-meshheading:21841129-Mice, Transgenic,
pubmed-meshheading:21841129-Protein Binding,
pubmed-meshheading:21841129-Receptors, Antigen, T-Cell,
pubmed-meshheading:21841129-Retroviridae Infections,
pubmed-meshheading:21841129-Reverse Transcriptase Polymerase Chain Reaction
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| pubmed:year |
2011
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| pubmed:articleTitle |
B cells and TCR avidity determine distinct functions of CD4+ T cells in retroviral infection.
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| pubmed:affiliation |
Division of Immunoregulation, Medical Research Council National Institute for Medical Research, The Ridgeway, London NW7 1AA, United Kingdom.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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