The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1999/11/1357/ $5.00
The Journal of Experimental Medicine, Volume 190, Number 9, November 1, 1999 1357-1362


Brief Definitive Report

Impaired Nk1.1 T Cell Development in Mice Transgenic for a T Cell Receptor β Chain Lacking the Large, Solvent-Exposed Cβ Fg Loop

Sylvie Degermanna, Giuseppina Sollamia, and Klaus Karjalainena

a Basel Institute for Immunology, CH-4005 Basel, Switzerland
Basel Institute for Immunology, Grenzacherstr. 487, CH-4005 Basel, Switzerland.41-61-605-136441-61-605-1249

degermann{at}bii.ch

A striking feature of the T cell receptor (TCR) β chain structure is the large FG loop that protrudes freely into the solvent on the external face of the Cβ domain. We have already shown that a transgene-encoded Vβ8.2+ TCR β chain lacking the complete Cβ FG loop supports normal development and function of conventional {alpha}/β T cells. Thus, the FG loop is not absolutely necessary for TCR signaling. However, further analysis has revealed that a small population of {alpha}/β T cells coexpressing NK1.1 are severely depleted in these transgenic mice. The few remaining NK1.1 T cells have a normal phenotype but express very low levels of TCR. We find that the TCR Vβ8.2+ chain lacking the Cβ FG loop cannot pair efficiently with the invariant V{alpha}14-J{alpha}281 TCR {alpha} chain commonly expressed by this T cell family. Consequently, fewer NK1.1 T cells develop in these mice. Our results suggest that expression of the V{alpha}14+ TCR {alpha} chain is particularly sensitive to TCR-β conformation. Development of NK1.1 T cells appears to need a TCR-β conformation dependent on the presence of the Cβ loop that is not necessarily required for assembly and function of TCRs on most {alpha}/β T cells.

Key Words: TCR • Cβ FG loop • mutagenesis • NK1.1 T cells • V{alpha}14


© 1999 The Rockefeller University Press


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