Literature DB >> 9688079

Participation of NK1.1+ T cells in the rejection of lpr alphabetaT cells when bone marrow cells of lpr mice are transplanted into B6 mice.

A Tsukahara1, H Kawamura, T Iiai, T Moroda, S Suzuki, T Tada, M Minagawa, N Musha, K Hatakeyama, T Abo.   

Abstract

When C57BL/6 (B6) mice were irradiated (9 Gy) and received bone marrow (BM) cells of B6-lpr/lpr mouse origin (i.e., lpr-->B6), all mice died within 6 days. In the irradiated B6 mice, radioresistant CD3 IL-2Rbeta+ NK cells and IL-2Rbeta+ CD3int cells (i.e., CD3int cells of extrathymic origin) remained, especially in the liver. There were two subsets, NK1.1+ and NK1.1-, among the IL-2Rbeta+ CD3int cells. However, the NK1.1+ subset (i.e., NK1.1- T cells) was much more radioresistant, and the majority of CD3int cells belonged to this subset in irradiated mice. The expansion of lymphocytes from injected BM cells did not occur in the irradiated B6 mice. However, such expansion did take place in irradiated B6-lpr/lpr mice injected with both BM cells of B6-lpr/lpr and B6 origin. As a result, the mice subjected to BM cells survived. Irradiated B6 mice were treated in vivo with anti-NK1.1 mAb or anti-asialoGM1 antibody to eliminate NK cells alone or both NK cells and NK1.1+ T cells. When irradiated B6 mice were pretreated with anti-NK1.1 mAb, the mice could survive. These results suggest that intact NK1.1+ T cells of extrathymic origin may recognize abnormal BM cells with the lpr gene and inhibit the expansion of lymphocytes, including abnormal double-negative CD4 8 cells, in B6-lpr/lpr mice. To inhibit the expansion of lymphocytes, mechanisms other than Fas ligand/Fas molecules on extrathymic T cells may be responsible.

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Year:  1998        PMID: 9688079     DOI: 10.1111/j.1348-0421.1998.tb02308.x

Source DB:  PubMed          Journal:  Microbiol Immunol        ISSN: 0385-5600            Impact factor:   1.955


  2 in total

1.  Activation of Valpha14(+) natural killer T cells by alpha-galactosylceramide results in development of Th1 response and local host resistance in mice infected with Cryptococcus neoformans.

Authors:  K Kawakami; Y Kinjo; S Yara; Y Koguchi; K Uezu; T Nakayama; M Taniguchi; A Saito
Journal:  Infect Immun       Date:  2001-01       Impact factor: 3.441

2.  A defect in interleukin 12-induced activation and interferon gamma secretion of peripheral natural killer T cells in nonobese diabetic mice suggests new pathogenic mechanisms for insulin-dependent diabetes mellitus.

Authors:  M Falcone; B Yeung; L Tucker; E Rodriguez; N Sarvetnick
Journal:  J Exp Med       Date:  1999-10-04       Impact factor: 14.307

  2 in total

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