| First Author | Zajac AJ | Year | 1995 |
| Journal | Int Immunol | Volume | 7 |
| Issue | 10 | Pages | 1545-56 |
| PubMed ID | 8562499 | Mgi Jnum | J:29449 |
| Mgi Id | MGI:76983 | Doi | 10.1093/intimm/7.10.1545 |
| Citation | Zajac AJ, et al. (1995) Natural killer cell activity in lymphocytic choriomeningitis virus-infected beta 2-microglobulin-deficient mice. Int Immunol 7(10):1545-56 |
| abstractText | We have investigated the induction and role of natural killer (NK) activity in lymphocytic choriomeningitis virus (LCMV)-infected beta 2-microglobulin-deficient (beta 2m-) mice. We demonstrate that LCMV infection is more effective than polyinosinic:polycytidylic acid (poly I:C) at stimulating NK activity in beta 2m- mice. In addition, beta 2m- NK cells respond poorly to in vitro treatment with IL-12. The target specificity of the virally induced NK cells is similar to that previously reported for chemically induced beta 2m- NK cells. In both cases they can lyse YAC-1 tumor cells but are unable to kill beta 2m- or beta 2m+ T cell blasts. We have also found that the time course of induction of NK and cytotoxic T lymphocyte (CTL) activity by LCMV in beta 2m- mice is delayed compared with normal mice. Maximal NK and CTL activity is attained at day 8 and 10 post-infection respectively in beta 2m- mice compared with day 4 and 6-8 in B6 mice. Whereas normal mice die approximately 7 days following intracranial infection with LCMV, the course of disease in beta 2m- mice is protracted and characterized by a marked loss of body weight. We show that although the CD4+ CTL response in these mice is intimately involved in mediating weight loss, the virus-induced NK cells do not appear to play a role in the disease. |
