Table 2.

Association of calcium (Ca²⁺) channels and various autoimmune diseases.

Disease	Channels and Cells	Effects
Rheumatoid arthritis	Upregulation of CRAC on T cells Upregulation of TRPV1 and TRPM8 on synoviocytes Activation of TRPV4 on synoviocytes Activation of TRPV2 on synoviocytes	Increase Ca2+ influx and NFAT transcription→ stimulation of secretion of inflammatory cytokines Activate caspase enzyme→ induce apoptosis of FLS Increase Ca2+ influx reduce→ chemokine production Increase intracellular Ca2+ concentration→ reduce joint inflammation
Systemic lupus erythematosus	Altered motility of Kv1.3 on T cells	Activate T cell proliferation and T cell-mediated autoimmune responses
Sjogren syndrome	Downregulation of CRAC on T regs Inhibition of TRPC3 on salivary gland	Reduce SOCE and Treg functions→ decrease salivary gland secretion Reduce Ca2+ influx→ reduce cell-mediated toxicity→ decrease inflammation
Psoriasis	Downregulation of TRPV6 on keratinocytes Downregulation of STIM1	Reduce Ca2+ influx→ inhibit keratinocyte differentiation and proliferation Reduce Ca2+ influx→ decrease chemotaxis of neutrophils
Multiple sclerosis	Upregulation of CRAC on T cells	Change Ca2+ entry Stimulate T cell activation and proliferation→ increase cytokine production

CRAC, Ca²⁺ release-activated Ca²⁺; NFAT, nuclear factor of activated T cell; TRPV, transient receptor potential vanilloid; TRPM, transient receptor potential melastatin; FLS, fibroblast-like synoviocyte; SOCE, store-operated Ca²⁺ entry; Tregs, regulatory T cells; TRPC, transient receptor potential canonical.