CD43 signals induce Type One lineage commitment of human CD4+ T cells

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• 作者：Oscar Ramírez-Pliego (1)
  Diana L Escobar-Zárate (1)
  Gemma M Rivera-Martínez (1)
  Mayte G Cervantes-Badillo (1)
  Fernando R Esquivel-Guadarrama (2)
  Gabriela Rosas-Salgado (2)
  Yvonne Rosenstein (3)
  M Angélica Santana (1)
  
• 刊名：BMC Immunology
• 出版年：2007
• 出版时间：December 2007
• 年：2007
• 卷：8
• 期：1
• 全文大小：2019KB
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• 作者单位：Oscar Ramírez-Pliego (1)
  Diana L Escobar-Zárate (1)
  Gemma M Rivera-Martínez (1)
  Mayte G Cervantes-Badillo (1)
  Fernando R Esquivel-Guadarrama (2)
  Gabriela Rosas-Salgado (2)
  Yvonne Rosenstein (3)
  M Angélica Santana (1)
  
  1. Facultad de Ciencias, Universidad Autónoma del Estado de Morelos, Av. Universidad 1001, Col. Chamilpa, 62210, Cuernavaca, Mexico
  2. Facultad de Medicina, Universidad Autónoma del Estado Morelos, Av. Universidad 1001, Col. Chamilpa, 62210, Cuernavaca, Mexico
  3. Instituto de Biotecnología Universidad Nacional Autónoma de México, Av. Universidad 2001, 62210, Col. Cuernavaca, Mexico
  
• ISSN：1471-2172

文摘

Background The activation and effector phenotype of T cells depend on the strength of the interaction of the TcR with its cognate antigen and additional signals provided by cytokines and by co-receptors. Lymphocytes sense both the presence of an antigen and also clues from antigen-presenting cells, which dictate the requisite response. CD43 is one of the most abundant molecules on the surface of T cells; it mediates its own signalling events and cooperates with those mediated by the T cell receptor in T cell priming. We have examined the role of CD43 signals on the effector phenotype of adult CD4+ and CD8+ human T cells, both alone and in the presence of signals from the TcR. Results CD43 signals direct the expression of IFNγ in human T cells. In freshly isolated CD4+ T cells, CD43 signals potentiated expression of the IFNγ gene induced by TcR activation; this was not seen in CD8+ T cells. In effector cells, CD43 signals alone induced the expression of the IFNγ gene in CD4+ T cells and to a lesser extent in CD8+ cells. The combined signals from CD43 and the TcR increased the transcription of the T-bet gene in CD4+ T cells and inhibited the transcription of the GATA-3 gene in both populations of T cells, thus predisposing CD4+ T cells to commitment to the T1 lineage. In support of this, CD43 signals induced a transient membrane expression of the high-affinity chains of the receptors for IL-12 and IFNγ in CD4+ T cells. CD43 and TcR signals also cooperated with those of IL-12 in the induction of IFNγ expression. Moreover, CD43 signals induced the co-clustering of IFNγR and the TcR and cooperated with TcR and IL-12 signals, triggering a co-capping of both receptors in CD4+ populations, a phenomenon that has been associated with a T1 commitment. Conclusion Our results suggest a key role for CD43 signals in the differentiation of human CD4+ T cells into a T1 pattern.