The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
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© The Rockefeller University Press, 0022-1007/1997/8/767/ $5.00
The Journal of Experimental Medicine, Volume 186, Number 5, August 29, 1997 767-775

Article

Allelic Exclusion in pT{alpha}-deficient Mice: No Evidence for Cell Surface Expression of Two T Cell Receptor (TCR)-β Chains, but Less Efficient Inhibition of Endogeneous Vβ-> (D)Jβ Rearrangements in the Presence of a Functional TCR-β Transgene

Anna Krotkova*, Harald von Boehmer{ddagger}, and Hans Jörg Fehling*

From the * Basel Institute for Immunology, CH-4005 Basel, Switzerland; and the {ddagger} Institut Necker, Institut National de la Santé et de la Recherche Medicale 373, F-75730 Paris Cedex 15, France

Although individual T lymphocytes have the potential to generate two distinct T cell receptor (TCR)-β chains, they usually express only one allele, a phenomenon termed allelic exclusion. Expression of a functional TCR-β chain during early T cell development leads to the formation of a pre-T cell receptor (pre-TCR) complex and, at the same developmental stage, arrest of further TCR-β rearrangements, suggesting a role of the pre-TCR in mediating allelic exclusion. To investigate the potential link between pre-TCR formation and inhibition of further TCR-β rearrangements, we have studied the efficiency of allelic exclusion in mice lacking the pre-TCR-{alpha} (pT{alpha}) chain, a core component of the pre-TCR. Staining of CD3+ thymocytes and lymph node cells with antibodies specific for Vβ6 or Vβ8 and a pool of antibodies specific for most other Vβ elements, did not reveal any violation of allelic exclusion at the level of cell surface expression. This was also true for pT{alpha}-deficient mice expressing a functionally rearranged TCR-β transgene. Interestingly, although the transgenic TCR-β chain significantly influenced thymocyte development even in the absence of pT{alpha}, it was not able to inhibit fully endogeneous TCR-β rearrangements either in total thymocytes or in sorted CD25+ pre-T cells of pT{alpha}–/– mice, clearly indicating an involvement of the pre-TCR in allelic exclusion.

Address correspondence to H.J. Fehling, Basel Institute for Immunology, Grenzacherstrasse 487, CH-4005 Basel, Switzerland. Phone: 41-61-605-1245; FAX: 41-61-605-1364; E-mail: fehling{at}bii.ch

1 Abbreviations used in this paper: BCR, B cell receptor; CS, calf serum; D, diversity; DN, double-negative; DP, double-positive; ES, embryonic stem; FSC, forward scatter; J, joining; PI, propidium iodine; pT{alpha}, pre-TCR{alpha}; SP, single-positive; SSC, side scatter; V, variable.


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