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International immunology, 2003-12, Vol.15 (12), p.1495-1504
2003
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Autor(en) / Beteiligte
Titel
Transforming growth factor-  inhibits human antigen-specific CD4+ T cell proliferation without modulating the cytokine response
Ist Teil von
  • International immunology, 2003-12, Vol.15 (12), p.1495-1504
Ort / Verlag
Oxford: Oxford Publishing Limited (England)
Erscheinungsjahr
2003
Quelle
Oxford Journals 2020 Medicine
Beschreibungen/Notizen
  • Transforming growth factor (TGF)-[beta] has been demonstrated to play a key role in the regulation of the immune response, mainly by its suppressive function towards cells of the immune system. In humans, the effect of TGF-[beta] on antigen-specific established memory T cells has not been investigated yet. In this study antigen-specific CD4<+< T cell clones (TCC) were used to determine the effect of TGF-[beta] on antigen-specific proliferation, the activation status of the T cells and their cytokine production. This study demonstrates that TGF-[beta] is an adequate suppressor of antigen-specific T cell proliferation, by reducing the cell-cycle rate rather than induction of apoptosis. Addition of TGF-[beta] resulted in increased CD69 expression and decreased CD25 expression on T cells, indicating that TGF-[beta] is able to modulate the activation status of in vivo differentiated T cells. On the contrary, the antigen-specific cytokine production was not affected by TGF-[beta]. Although TGF-[beta] was suppressive towards the majority of the T cells, insensitivity of a few TCC towards TGF-[beta] was also observed. This could not be correlated to differential expression of TGF-[beta] signaling molecules such as Smad3, Smad7, SARA (Smad anchor for receptor activation) and Hgs (hepatocyte growth factor-regulated tyrosine kinase substrate). In summary, TGF-[beta] has a pronounced inhibitory effect on antigen-specific T cell proliferation without modulating their cytokine production.
Sprache
Englisch
Identifikatoren
ISSN: 1460-2377, 0953-8178
eISSN: 1460-2377
DOI: 10.1093/intimm/dxg147
Titel-ID: cdi_proquest_journals_195039781
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