Figure legends
Figure 1. Autoreactive T cells pass through negative selection due to Fas-deficiency 27, 28. Fas-deficiency may result in the generation of autoreactive B cells 59, 60. The expression of CD138 in T cells induces apoptosis defects and leads to the accumulation of autoreactive T cells 14. Autoreactive CD4+ T cells further activate the expression of MHC-II in autoreactive B cells with self-antigens 7, 14, 30 and also promote the formation of autoreactive plasma cells that secrete autoantibodies.
Figure 2. DN T cells derived from CD4 38, 39 and CD826, 35, 40, 41 positive cells. Single-positive T cells for which CD4+ T cells or CD8+ T cells downregulate their coreceptor (CD4 or CD8, respectively); they may convert into DN T cells10. Expression of CD138 induces apoptosis defects in DN T cells and results in their accumulation.
Figure 3. In healthy people, pDCs and Breg cells build an auto-regulatory feedback mechanism in the immune system22. However, the regulatory feedback mechanism is compromised in SLE 22, which breaks the balance between immune response and immune tolerance.
Figure 4. Population of MDSCs will expand in response to inflammatory environments, such as increased cytokines (including IFN-γ, IL-6, and TNF-α 83, 95), thus suppressing inflammation83. In SLE, sustained increases in the levels of cytokines (such as TNF-α, IL-6, and IFN-γ) promote the differentiation of MDSCs into macrophage and dendritic cells 89, 90; this breaks the balance between self-tolerance induced by MDSCs and inflammation induced by cytokines.
Figure 1