HISTOPATHOLOGICAL CHANGES IN EXOCRINE GLANDS OF MURINE TRANSPLANTATION CHIMERAS. I: THE DEVELOPMENT OF SJöGREN'S SYNDROME-LIKE CHANGES SECONDARY TO GVH INDUCED LUPUS SYNDROME

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Abstract
Sjögren's syndrome (SS) is a connective tissue disease characterized by general affection of exocrine glands. The three main components of SS are: dry eyes, dry mouth, and other connective tissue disease. When only two of these, dry eyes and dry mouth, are present, the disease is designated primary SS. In the presence of the third component, most commonly SLE or RA, with one or both of the two first components the disease is designated secondary SS. In murine transplantation chimeras, we have demonstrated the development of both primary and secondary SS depending upon the mouse strains used. We transferred large numbers of viable leucocytes from homozy-gotic donors to heterozygotic recipients. When DBA/2 mice were used as donors, a full-developed SLE-syndrome, with autoantibodies against native DNA, nuclear antigens, and red blood cells was observed. We found immune deposits in skin (“lupus band”) and kidneys, immune complex glomerulonephritis (ICGN), proteinuria, ascites, and hepatosplenomegaly. In later stages, we found a generalized dacryoadenitis. In the kidneys we found interstitial nephritis, and occasionally “half-moon” nephritis. In skin, immune deposits were demonstrated in intercellular spaces. These findings are similar to those found in patients with Sjogren's syndrome secondary to SLE. The murine transplantation chimera is therefore an experimental model for spontaneous autoimmune diseases.