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. Author manuscript; available in PMC: 2016 Sep 1.
Published in final edited form as: Semin Nephrol. 2015 Sep;35(5):396–409. doi: 10.1016/j.semnephrol.2015.08.002

Figure 2.

Figure 2

Adaptive immunity processes contribute to lupus nephritis. A. T-lymphocyte activation. Nuclear antigens are phagocytosed, processed, and presented in the context of MHC by APC, which then interacts with the TCR on T-lymphocytes and activates downstream signaling events (Signal 1). Co-stimulatory molecules from the CD28 and TNFR families engage to prevent anergy and amplify the MHCII/TCR response in CD4 T-helper cells (Signal 2). Downstream signals lead to the secretion of cytokines (Signal 3), which then interact with transcriptional regulators to drive T-lymphocyte differentiation pathways. B. B-lymphocyte activation. Nuclear antigens stimulate the BCR, activating the BCR signaling complex that results in downstream signaling events. Co-stimulatory molecules, including CD40 and TLRs, synergize with the BCR to amplify B-lymphocyte activation.

*Genes/molecules with genetic variants associated with lupus nephritis