دورية أكاديمية

Suppression of HIV-specific and allogeneic T cell activation by human regulatory T cells is dependent on the strength of signals.

التفاصيل البيبلوغرافية
العنوان: Suppression of HIV-specific and allogeneic T cell activation by human regulatory T cells is dependent on the strength of signals.
المؤلفون: Amanda K Antons, Rui Wang, Spyros A Kalams, Derya Unutmaz
المصدر: PLoS ONE, Vol 3, Iss 8, p e2952 (2008)
بيانات النشر: Public Library of Science (PLoS), 2008.
سنة النشر: 2008
المجموعة: LCC:Medicine
LCC:Science
مصطلحات موضوعية: Medicine, Science
الوصف: Regulatory T cells (Tregs) suppress immune responses against both self and non-self antigens. Tregs require activation through the T cell receptor (TCR) and IL-2 to exert their suppressive functions. However, how strength of TCR signals modulate the potency of Treg-mediated suppression of antigen-specific T cell activation remain unclear. We found that both strength of TCR signals and ratios of Tregs to target cells, either through superantigen, allogeneic antigens or HIV-specific peptides, modified the suppressive ability of Tregs. While human Tregs were able to mediate suppression in the presence of only autologous antigen-presenting cells, this was much less efficient as compared to when Tregs were activated by allogeneic dendritic cells. In another physiologically relevant system, we show that the strength of peptide stimulation, high frequency of responder CD8+ T cells or presence of high IL-2 can override the suppression of HIV-specific CD8+ T cells by Tregs. These findings suggest that ratios and TCR activation of human Tregs, are important parameters to overcome robust immune responses to pathogens or allogeneic antigens. Modulating the strength of T cell signals and selective enhancement or depletion of antigen-specific Tregs thus may have implications for designing potent vaccines and regulating immune responses during allogeneic transplantation and chronic infections.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1932-6203
Relation: http://europepmc.org/articles/PMC2490715?pdf=render; https://doaj.org/toc/1932-6203
DOI: 10.1371/journal.pone.0002952
URL الوصول: https://doaj.org/article/bbc87d2efb754b36b6c87af7f663186c
رقم الأكسشن: edsdoj.bbc87d2efb754b36b6c87af7f663186c
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:19326203
DOI:10.1371/journal.pone.0002952