Systemic lupus erythematosus (SLE) has a pathophysiology that involves B, T, and dendritic cells, as well as inflammatory cytokines such as IFN-1, IL-6, and BAFF. By understanding the evolving science behind this complex disease, we can begin to unlock the nature of SLE.1-7

BAFF, B-cell–activating factor; IFN-1, type 1 interferon; IL, interleukin; SLE, systemic lupus erythematosus.

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Learn about the heterogeneity of SLE

References:

1. Crow MK. Type I interferon in the pathogenesis of lupus. J Immunol. 2014;192(12):5459-5468. 2. Wahren-Herlenius M, Dörner T. Immunopathogenic mechanisms of systemic autoimmune disease. Lancet. 2013;382(9894):819-831. 3. Kim J-M, Park S-H, Kim H-Y, et al. A plasmacytoid dendritic cells–type I interferon axis is critically implicated in the pathogenesis of systemic lupus erythematosus. Int J Mol Sci. 2015;16(6):14158-14170. 4. Lauwerys BR, Ducreux J, Houssiau FA. Type I interferon blockade in systemic lupus erythematosus: where do we stand? Rheumatology (Oxford). 2014;53(8):1369-1376. 5. Hoffman RW, Merrill JT, Alarcón-Riquelme MM, et al. Gene expression and pharmacodynamic changes in 1,760 systemic lupus erythematosus patients from two phase III trials of BAFF blockade with tabalumab. Arthritis Rheumatol. 2017;69(3):643-654. 6. Rönnblom L, Elkon KB. Cytokines as therapeutic targets in SLE. Nat Rev Rheumatol. 2010;6(6):339-347. 7. Allen ME, Rus V, Szeto GL. Leveraging heterogeneity in systemic lupus erythematosus for new therapies. Trends Mol Med. 2021;27(2):152-171.

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