Abstract
Ions, such as calcium, magnesium, potassium and sodium ions, are critically involved in the development and function of various tissues. Among these ions, calcium is known to function as second messenger to regulate a variety of immune cell functions including cytokine production, cytotoxicity, chemotaxis, and differentiation to effector cells. Intracellular concentration of calcium is increased after the engagement of immune receptors such as T-cell receptor and Fc receptor and strictly controlled by a network of calcium-permeable channels, transporters, and pumps. Among various mechanisms of extracellular calcium entry in lymphocytes, store-operated calcium (SOC) entry through calcium–release-activated calcium (CRAC) channels is known to be the predominant mechanism of antigen receptor-activated increase in intracellular calcium levels. Induction of calcium entry via CRAC channels is mediated by two molecular components, ORAI1, a subunit of the CRAC channels expressed in the plasma membrane, and stromal interaction molecule (STIM)1, a calcium sensor in the endoplasmic reticulum. Dysregulation of SOC entry has been reported to induce immunological and nonimmunological diseases. In this chapter, we first introduce the molecular mechanism of SOC entry, and then describe the physiological consequences of impaired SOC entry in human and mouse. Finally, the mechanism of the development of autoimmune diseases by the loss of SOC entry is described.
Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
