RT Journal Article
T1 TCR signal strength controls thymic differentiation of discrete proinflammatory gamma-delta T cell subsets
A1 Muñoz Ruiz, Miguel
A1 Ribot, Julie C.
A1 Grosso, Ana R.
A1 Gonçalves Sousa, Natacha
A1 Pamplona, Ana
A1 Pennington, Daniel J.
A1 Regueiro González-Barros, José Ramón
A1 Fernández Malavé, Edgar Gonzalo
A1 Silva Santos, Bruno
AB The mouse thymus produces discrete gd T cell subsets that make either interferon-g (IFN-g) 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 gd T cells. CD3DH mice had normal numbers and phenotypes of ab thymocyte subsets, but impaired differentiation of fetal Vg6+ (but not Vg4+) IL-17- producing gd T cells and a marked depletion of IFN-g-producing CD122+ NK1.1+ gd T cells throughout ontogeny. Adult CD3DH mice showed reduced peripheral IFN-g+ gd 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 gd T cell subsets and their impact on pathophysiology.
PB Nature Publishing Group
SN 1529-2908
YR 2016
FD 2016-04-04
LK https://hdl.handle.net/20.500.14352/23904
UL https://hdl.handle.net/20.500.14352/23904
LA spa
NO Muñoz Ruiz, M., Ribot, J. C., Grosso, A. R. et al. «TCR Signal Strength Controls Thymic Differentiation of Discrete Proinflammatory Γδ T Cell Subsets». Nature Immunology, vol. 17, n.o 6, junio de 2016, pp. 721-27. DOI.org (Crossref), https://doi.org/10.1038/ni.3424.
NO Unión Europea
NO Unión Europea
NO Ministerio de Economía, Comercio y Empresa (España)
NO Comunidad de Madrid
NO Fundacion Lair
DS Docta Complutense
RD 5 abr 2025