ArticlePloS one2013
STAT3 signaling induces the differentiation of human ICOS(+) CD4 T cells helping B lymphocytes.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 17 citations in OpenAlex.
- Prolactin Increases the Frequency of Follicular T Helper Cells with Enhanced IL21 Secretion and OX40 Expression in Lupus-Prone MRL/lpr Mice.Journal of immunology research · 2021Article
- The calcium-binding protein S100B reduces IL6 production in malignant melanoma via inhibition of RSK cellular signaling.PloS one · 2021Article
- Signal Transducer and Activator of Transcription 3 Control of Human T and B Cell Responses.Frontiers in immunology · 2018Review
- Human T Follicular Helper Cells in Primary Immunodeficiency: Quality Just as Important as Quantity.Journal of clinical immunology · 2016Review
- Reducing the standard deviation in multiple-assay experiments where the variation matters but the absolute value does not.PloS one · 2013Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The generation of high-affinity antibodies and the development of B cell memory are dependent on the help provided by CD4 T cells. Mouse studies indicate that STAT3 signaling in CD4 T cells promotes the acquisition of the B cell help function. However, the role of STAT3 in humans has been controversial. In this study, we show that IL-6 and other STAT3 activating cytokines (IL-21 and IL-27) induce the differentiation of CD4 T cells promoting antibody production by B cells. The acquisition of B cell stimulating properties by naive cord blood CD4 T cells required the STAT3-dependent expression of ICOS and IL-21. Gene reporter and ChIP experiments unambiguously demonstrated that upon IL-6 stimulation, STAT3 induces the transcription of the ICOS gene through direct recruitment to the proximal promoter region indicating that STAT3 acts in part through the direct activation of the ICOS gene.
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Registered trials
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