A PROTECTIVE ROLE OF GAMMA-DELTA T-CELLS IN PRIMARY INFECTION WITH LISTERIA-MONOCYTOGENES IN AUTOIMMUNE NONOBESE DIABETIC

We investigated the host defense mechanism in primary infection with L isteria monocytogenes in non-obese diabetic (NOD) mice at pre-diabetic stage showing an impaired responsiveness of the alpha beta T cells to T-cell receptor (TCR) triggering. The NOD mice showed a deteriorated resistance at the late stage after an intraperitoneal infection with L . monocytogenes compared with BALB/c and C57BL/6 mice as assessed by b acterial growth in organs. Consistent with our previous findings, a pr ominent increase in number of gamma delta T cells was evident at the e arly stage after infection, while generation of Listeria-specific alph a beta T cells was impaired in these mice. In vivo administration of a nti-TCR gamma delta monoclonal antibody (mAb) allowed L. monocytogenes to grow exaggeratedly in the NOD mice. These results imply that gamma delta T cells may be mainly involved in protection against primary in fection with L. monocytogenes in NOD mice.