Lupus pathogenesis (Homo sapiens)

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Systemic lupus erythematosus (SLE) is an autoimmune disease in which the body’s immune system mistakenly attacks its own tissues. It can lead to lupus nephritis, where the kidneys become inflamed. This causes impaired kidney function and, in severe cases, kidney failure. Lupus has an incidence of around 5 per 100,000 person-years, and affects women much more frequently than men.

The development of lupus nephritis involves a complex interplay among B cells, T cells, dendritic cells (DCs), and other immune components. Key pathogenic mechanisms include:

1. Overactive B cells produce excessive autoantibodies, leading to the formation of immune complexes that deposit in the kidneys. These deposits trigger complement activation and subsequent inflammation.

2. Autoreactive B cells present self-antigens to T cells, promoting persistent immune dysregulation and the release of pro-inflammatory cytokines.

3. Dendritic cells display abnormal recognition and presentation of self-antigens, which initiates and sustains autoimmune responses targeting renal tissues.

4. B cell differentiation into plasma cells is dysregulated, resulting in continuous production of nephritogenic autoantibodies.

Understanding these immunopathogenic processes is critical for the development of targeted therapies aimed at preventing or reversing the progression of lupus nephritis.

Inspired by [Figure 2 in Su et al. (2024)](https://pmc.ncbi.nlm.nih.gov/articles/PMC11522254/).