Effect of antibodies to intercellular adhesion molecule (ICAM)-1 and lymphocyte function-associated antigen (LFA)-1 on cytokine mRNA expression in reovirus type-2-triggered autoimmune insulitis in suckling DBA/1 mice.

Interleukin (IL)-12 in the presence of IL-18 induces T helper (Th) 1 dominated systemic immune reactions, such as those that occur in autoimmune insulitis in suckling mice infected with reovirus type-2 (Reo-2). The role of intercellular adhesion molecule (ICAM)-1 and lymphocyte function-associated antigen (LFA)-1 on the induction of cytokines responsible for Reo-2-triggered insulitis with impaired glucose tolerance (IGT) was examined. One-day-old DBA/1 mice infected with Reo-2 intraperitoneally (i.p.) were treated i.p. with monoclonal antibodies (mAbs) against ICAM-1 and LFA-1 (ICAM-1/LFA-1) at 5 days post-infection (d.p.i.). At 10 d.p.i., the administration of the mAbs was seen to have prevented the development of insulitis with IGT. This was associated with a decrease in the mRNA expression for IL-12(p40) and IL-18 by splenic cells. The present study suggests that ICAM-1/LFA-1 may be required for the differentiation of Th0 cells to Th1 cells, which mediate insulitis with IGT in Reo-2-infected suckling mice.