[Immunoregulative effect of NK1.1+ cells on the development of experimental autoimmune myasthenia gravis]

To investigate the effect and immuoregulative mechanisms of NK1.1(+) cells on the development of experimental autoimmune myasthenia gravis (EAMG).

The NK1.1(+) cells were depleted by intraperitoneal (i.p.) administration of anti-mouse NK1.1 mAb to C57BL/6 mice. Mice were immunized subcutaneously with AChR in CFA. The incidence and severity of EAMG was determined according to the Lennon disease symptoms grading. IFN-gamma and IL-4 in MNCs culture medium were measured by ELISA. AChR IgG of serum was measured by radioimmunoassay. In some experiments, the anti-IFN-gamma mAb was injected (i.p.) to neutralize IFN-gamma.

The onset of EAMG was delayed and the severity was decreased obviously in NK1.1(+) cell-depleted mice. However, depletion of NK1.1(+) cells after immunization had no impact on the development of EAMG. Depletion of NK1.1(+) cells could significantly reduce the expression of AChR-specific antibody as well as the production of IFN-gamma. The development of EAMG and production of AChR specific Ab in NK1.1(+) cell-depleted mice were decreased obviously after treating with anti-IFN-gamma antibody.

NK1.1(+) cells are involved in the early EAMG, and NK1.1(+) cells could enhance the production of IFN-gamma released by AChR-specific T cells as well as the AChR-specific antibodies, which may enhance the outcome of EAMG.