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TCR signal strength controls thymic differentiation of discrete proinflammatory γδ T cell subsets.

Muñoz-Ruiz, Miguel; Ribot, Julie C; Grosso, Ana R; Gonçalves-Sousa, Natacha; Pamplona, Ana; Pennington, Daniel J; Regueiro, José R; Fernández-Malavé, Edgar; Silva-Santos, Bruno.
Nat Immunol ; 17(6): 721-727, 2016 06.
Artículo en Inglés | MEDLINE | ID: mdl-27043412
The mouse thymus produces discrete γδ T cell subsets that make either interferon-γ (IFN-γ) or interleukin 17 (IL-17), but the role of the T cell antigen receptor (TCR) in this developmental process remains controversial. Here we show that Cd3g(+/-) Cd3d(+/-) (CD3 double-haploinsufficient (CD3DH)) mice have reduced TCR expression and signaling strength on γδ T cells. CD3DH mice had normal numbers and phenotypes of αß thymocyte subsets, but impaired differentiation of fetal Vγ6(+) (but not Vγ4(+)) IL-17-producing γδ T cells and a marked depletion of IFN-γ-producing CD122(+) NK1.1(+) γδ T cells throughout ontogeny. Adult CD3DH mice showed reduced peripheral IFN-γ(+) γδ T cells and were resistant to experimental cerebral malaria. Thus, TCR signal strength within specific thymic developmental windows is a major determinant of the generation of proinflammatory γδ T cell subsets and their impact on pathophysiology.