DNMT-1 inhibition due to CS-induced oxidative stress increases expression of lymphocyte function-associated antigen-a heterodimer composed of CD11a and CD18 [LFA (CD11a/CD18)] and CD70 in T cells and changes antigen-specific CD4+ T helper cells into auto-reactive pro-inflammatory cells, which respond to self-class 2 MHC molecules without added antigens and kill autologous macrophages, resulting in lupus-like autoimmunity [108, 116]. This evidence concerns the gene ITGB2 and systemic lupus erythematosus.