| First Author | Beutner U | Year | 1997 |
| Journal | Eur J Immunol | Volume | 27 |
| Issue | 4 | Pages | 928-34 |
| PubMed ID | 9130646 | Mgi Jnum | J:40235 |
| Mgi Id | MGI:87578 | Doi | 10.1002/eji.1830270419 |
| Citation | Beutner U, et al. (1997) Natural killer-like T cells develop in SJL mice despite genetically distinct defects in NK1.1 expression and in inducible interleukin-4 production. Eur J Immunol 27(4):928-34 |
| abstractText | An unusual subset of mature T cells expresses natural killer (NK) cell-related surface markers such as interleukin-2 receptor beta (IL-2R beta; CD122) and the polymorphic antigen NK1.1. These ''NK-like'' T cells are distinguished by their highly skewed V alpha and V beta repertoire and by their ability to rapidly produce large amounts of IL-4 upon T cell receptor (TCR) engagement. The inbred mouse strain SJL (which expresses NK1.1 on its NK cells) has recently been reported to lack NK1.1(+) T cells and consequently to be deficient in IL-4 production upon TCR stimulation. We show here, however, that SJL mice have normal numbers of IL-2R beta(+) T cells with a skewed V beta repertoire characteristic of ''NK-like'' T cells. Furthermore lack of NK1.1 expression on IL-2R beta(+) T cells in SJL mice was found by backcross analysis to be controlled by a single recessive gene closely linked to the NKR-P1 complex on chromosome 6 (which encodes the NK1.1 antigen). Analysis of a panel of inbred mouse strains further demonstrated that lack of NK1.1 expression on IL-2 beta(+) T cells segregated with NKR-P1 genotype (as assessed by restriction fragment length polymorphism) and thus was not restricted to the SJL strain. In contrast, defective TCR induced IL-4 production (which appeared to be a unique property of SJL mice) seems to be controlled by two recessive genes unlinked to NKR-P1. Collectively, our data indicate that ''NK-like'' T cells develop normally in SJL mice despite genetically distinct defects in NK1.1 expression and inducible IL-4 production. |
