The Journal of Experimental Medicine
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Published online
doi:10.1084/jem.20070550
The Journal of Experimental Medicine, Vol. 204, No. 9, 2115-2129
The Rockefeller University Press, 0022-1007 $30.00
© Laky et al.
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Article

 Presenilins regulate {alpha}β T cell development by modulating TCR signaling

Karen Laky and B.J. Fowlkes

Laboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892

CORRESPONDENCE B.J. Fowlkes: bfowlkes{at}nih.gov

TCR{alpha}β signaling is crucial for the maturation of CD4 and CD8 T cells, but the role of the Notch signaling pathway in this process is poorly understood. Genes encoding Presenilin (PS) 1/2 were deleted to prevent activation of the multiple Notch receptors expressed by developing thymocytes. PS1/2 knockout thymocyte precursors inefficiently generate CD4 T cells, a phenotype that is most pronounced when thymocytes bear a single major histocompatibility complex (MHC) class II–restricted T cell receptor (TCR). Diminished T cell production correlated with evidence of impaired TCR signaling, and could be rescued by manipulations that enhance MHC recognition. Although Notch appears to directly regulate binary fate decisions in many systems, these findings suggest a model in which PS-dependent Notch signaling influences positive selection and the development of {alpha}β T cells by modifying TCR signal transduction.

Abbreviations used: CSL, CBF1/Su(H)/Lag-1; dn, dominant negative. DN, double negative; dnMAML, dn Mastermind-like; DP, NIAID, National Institute of Allergy and Infectious Disease; NICD, Notch intracellular domain; PE, phycoerythrin; PS, Presenilin; SP, single positive; Tg, transgene.

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