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G. Jiang, Y. Bian, Y. Ke, Y. Wang, H. J. Kaplan, D. Sun, H. Shao; Both Autoreactive T cells and Autoantibodies Contribute to the Experimental Autoimmune Keratoconjunctivitis Sicca (KCS) Induced by Newly Characterized Autoantigen, KlK1b22. Invest. Ophthalmol. Vis. Sci. 2009;50(13):2637.
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© ARVO (1962-2015); The Authors (2016-present)
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.
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.
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.
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.
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