@article {Munoz-ruiz2016,
	title = {TCR signal strength controls thymic differentiation of discrete proinflammatory γδT cell subsets},
	journal = {Nature immunology},
	number = {April},
	year = {2016},
	abstract = {<p>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 αβ 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.</p>
},
	doi = {10.1038/ni.3424},
	url = {https://doi.org/10.1038/ni.3424},
	author = {Mu{\~n}oz-ruiz, Miguel and Ribot, Julie C and Grosso, Ana R and Gon{\c c}alves-sousa, Natacha and Pamplona, Ana and Pennington, Daniel J and Regueiro, Jos{\'e} R and Fern{\'a}ndez-malav{\'e}, Edgar and Silva-santos, Bruno}
}
