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It is a crucial nutrient for red blood cells and nerve cells, and it helps your body grow and repair tissues

In SLE, CD4 + T-cells exhibit hyperactivation with reduced activation thresholds ( + CXCR3 + T-cell arterial infiltration ( + CCR5 + T-cells accumulate in SLE patients with carotid AS, demonstrating CCR5-mediated plaque homing ( + (tissue migration) and CCR5 + (plaque recruitment) subsets synergistically accelerate AS through complementary pathways ( Figure 4 Follicular helper T-cells (Tfh) exacerbate AS via major histocompatibility complex II (MHCII)-dependent B-cell differentiation into IgG-secreting plasma cells ( Imbalanced regulatory T-cell (Treg)/effector T-cell (Teff) ratios correlate with AS progression ( hi CD4 + and exhausted/activated CD8 + T-cells infiltrate SLE vascular lesions ( Other T-cell subsets, such as CD3 + CD31 + CXCR4 + angiogenic T-cells (Tang), aid vascular endothelium repair during AS ( + Tang cell levels in blood may signal endothelial damage and cardiovascular risks ( Metabolically reprogrammed CD4 + T-cells exhibit enhanced glycolysis via pyruvate kinase M2 (PKM2) activation, releasing pro-inflammatory cytokines ( 2.5 B-cell dysfunction B-cells and their autoantibodies are key in SLE-induced AS, as shown in Figure 4

By synthesizing recent research findings, this chapter aims to provide fresh insights into the nuanced interplay among cysteine, homocysteine, and disease progression

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