Histopathological changes in exocrine glands of murine transplantation chimeras. II: Sjögren's syndrome-like exocrinopathy in mice without lupus nephritis. A model of primary Sjögren's syndrome.

Autoimmune reactions are evoked in hybrid mice after induction of a chronic graft-versus-host reaction by transfer of viable leucocytes from one of the parental strains to non-irradiated F1 recipients. We have previously demonstrated an SLE-like syndrome early in the reaction, with an additional Sjögren's syndrome-like glandular affection occurring later. In this study, we used Balb/c mice as donors and Balb/cxCBA/H-T6 F1 hybrids as recipients. We found serum autoantibodies characteristic of SLE after 9 weeks but not after 20 weeks. No clinical signs of disease were seen at any time. After prolonged studies (5 months), we found heavy inflammation in Harderian, salivary, and tear glands. All animals survived the entire length of the experiment without signs of renal failure. The pathological manifestations: lymphocytic infiltration of exocrine glands, and enlargement of lymph nodes, are similar to those seen in patients with Sjögren's syndrome. This murine transplantation chimera may be a useful experimental model for primary Sjögren's syndrome.