Abstract
SLE, as an autoimmune disease, involves tissue inflammation of multiple organs, including the kidney. Lupus nephritis (LN) is an immune complex glomerulonephritis that develops as a frequent and potentially dismal manifestation of SLE. Lymphangiogenesis is the proliferation of pre-existing lymphatic vessels (LVs), which regulate tissue fluid homeostasis and immune cell trafficking, responding to the tissue environment. In this study, we have evaluated the lymphangiogenesis in the resiquimod-induced murine lupus nephritis model.
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