| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1988: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1987: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Research Abstract |
In this study, MRL/Mp-lpr/lpr (MRL/l) mice were used and killed at 6, 8, 12, 20 and more than 24 weeks after birth for immunohistochemical examinations of lesions in the submandibular gland, sublingual gland, tongue, submandibular lymph nodes, lung, kidney, and spleen et al. Auto-antibodies in the serum were investigated in some MRL/l mice. Examination of peripheral t cell subsets by different Lyt phenotypes was mainly performed by the avidin-biotin peroxidase complex method using anti-mouse monoclonal antibodies (becton discinson co. ltd.). the fluorescent antibody method was used to detect immune complex and c_3 fragment and antinuclear antibody in the serum. soluble nuclear antigen was detected by ouchte-rlony assay. the tissular disorder of the oral cavity in mrl/l mice was revealed to be a symptom of immune complex disease caused by the proliferation of genetically determined helper T lymphocytes (Thy-1, 2^+, Lyt-1^+), regulated by lpr genes. It was demonstrated that polyclonal B cell activation provoked by the focal infiltration of lymphocytes (Lyt-1^+) emerging in the parenchyma at the early stage, and deposition of immune complex caused by production of autoantibody plays an important part in the appearance and progression of granulomatous angiitis in the submandibular gland. At the same time, deposition of immune complex and abnormal macrophage function were found to be important causes of granulomatous angiitis manifestating in the tongue.
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