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