SLE, as an autoimmune disease, involves tissue inflammation of multiple organs, including the kidney. Lupus nephritis (LN) is thought to be an immune complex glomerulonephritis that develops as a frequent and potentially dismal manifestation of SLE. Lupus nephritis (LN) is thought to be 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, I have evaluated the lymphangiogenesis in the kidney and renal draining lymph nodes in the murine lupus nephritis model, and the relationship between pathological renal lymphangiogenesis and tertiary lymphoid structures in the lupus nephritis. Thus, I performed a mouse model for resiquimod-induced lupus nephritis model in 8-week-old BALB/c mice. My data show that, compared to the control group, renal mRNA expression of LYVE-1, VEGFR3, and other marks for lymphatic vessels remarkably increased following the resiquimod administration. Additionally, the increased expression of organized lymphoid organs-related homeostatic chemokines and adhesion molecules, and the presence of T and B cell aggregates, germinal centers (GCs) reminiscent of the secondary lymphoid organs founded around the pathological LVs, and the formation of high endothelial vessels (HEVs) within the tertiary lymphoid tissues (TLTs) indicated that lymphangiogenesis might have a role in maintaining immune responses and the organization of TLTs during the development of murine LN.