Abstract
Purpose: :
We have recently identified an autoantigen KLK1b22 from the lacrimal and salivary glands, which could induce KCS by either immunization with this antigen or adoptive transfer of this antigen specific T cells. In current study, we wanted to determine whether this novel antigen can be recognized by B cells and whether the disease can be induced by the transfer of serum from diseased rats.
Methods: :
Lewis rats were immunized with Klk1b22. Specific T cell responses and antibody production were kinetically examined. Serum or T cells derived from immunized rats were injected into naïve rats. The diseases were then compared clinically and pathologically.
Results: :
Anti-Klk1b22 Ab was detected in the serum of immunized rats starting 2 weeks till 30 weeks post-immunization. The subtypes of Ab were both IgG2a and IgG1, with a 2:1 ratio of IgG2a to IgG1. Serum transferred rats developed KCS. Compared to the histology of T cell transferred KCS, which showed a focal inflammatory cell infiltration, the lacrimal glands of serum transferred rats demonstrated atrophy and apoptosis of the acinar cells and ductal epithelium starting at 9 days post transfer. We have also observed that rats receiving serum containing anti-Klk1b22 antibody generated KLK1b22-specific T cells.
Conclusions: :
Both autoreactive T and B cells contribute to the Klk1b22 induced autoimmunity in the lacrimal glands, which should provide a useful model for understanding the immune mechanisms of T-B interactions in the pathogenesis of clinical KCS.
Keywords: autoimmune disease • lacrimal gland • cornea: tears/tear film/dry eye