| Literature DB >> 1985122 |
J E Riggs1, R S Stowers, D E Mosier.
Abstract
Mice with the autosomal recessive severe combined immune deficiency (scid) mutation lack mature lymphocytes because of defective joining of T cell receptor and immunoglobulin (Ig) gene segments. Penetrance of this mutation is incomplete since 10-25% of SCID mice produce some T or B lymphocytes. This "leaky" phenotype could be due to a reversion of the mutation in some mice or to a constant, low frequency of functional lymphocytes generated in all SCID mice with variable survival of such cells. We report here that all SCID mice can be stimulated to produce functional B cells by the transfer of normal neonatal, but not adult, T cells. T cell-induced rescue of C.B-17scid B cells results in high levels of Ig expressing the Ighb allotype of the SCID recipient. These results show that all SCID mice generate some functional B cells, the majority of which do not survive in the absence of a subset of T cells present in high frequency in the neonate.Entities:
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Year: 1991 PMID: 1985122 PMCID: PMC2118747 DOI: 10.1084/jem.173.1.265
Source DB: PubMed Journal: J Exp Med ISSN: 0022-1007 Impact factor: 14.307