Fig. 3.

Recently elucidated mechanisms and their interactions involved in systemic lupus erythematosus (SLE) modification. Regulation of innate response and enhanced pro-inflammatory cytokines secretion through polymorphism have been recently identified in SLE. Role of mitochondrial dysfunction and associated oxidative stress in metabolic alterations and their impact on immune cell activity and differentiation have been majorly focused in recent studies on SLE. Novel signaling mechanisms have also been elaborated related to metabolic fitness of T cell and their importance in SLE immunobiology. Implications of inflammatory cytokines rich microenvironment on immune cell differentiation specifically, on T cells has been recently focused in SLE related studies. SNP Single nucleotide polymorphism, TLR toll- like receptor, HIF-1α Hypoxia inducing factor 1α, PER2 Period circadian protein homolog 2, DNMT3B DNA-methyltransferase 3 beta, VDAC voltage- dependent anion channel, EZH2 Enhancer of zeste homolog 2, PKC protein kinase C, STAT6 signal transducer and activator of transcription 6, GATA3 GATA binding protein 3, pDC plasmacytoid dendritic cells, ITAM Immunoreceptor tyrosine-based activation motif, ZAP-70 Zeta chain associated protein kinase 70 mTORC1 mammalian target of rapamycin complex 1, IRAK interleukin-1 receptor-associated kinases, IFNα interferon α, Ras-MPK Ras-mitogen-activated protein kinase, Cxcl10 C-X-C motif chemokine ligand 10, ISGs interferon stimulated genes, CD3 cluster of differentiation 3