A recent study at NYU School of Medicine has provided a new perspective on how our bodies, specifically T-cells, respond to a viral infection. It turns out that calcium is extremely important in helping T-cells proliferate by activating a transcription factor called NFAT, which turns on genes that regulate the uptake and breakdown of glucose. Moreover, a specific calcium channel present in T-cells, or SOCE (store-operated calcium entry), is directly responsible for regulating and activating NFAT, which means that SOCE, or calcium flow into these T-cells, are directly responsible for the breakdown of glucose that is required for T-cell proliferation. This new finding helps explain how drugs like tacrolimus help fight autoimmune diseases like lupus and rheumatoid arthritis, (diseases where an oversensitive immune system ends up attacking the body's own tissues) since it shuts down the NFAT pathway therefore inhibiting glucose usage and T-cell proliferation. Furthermore, the research team also found that human patients with deficiencies in these calcium channels did not have T-cells that were proliferating or taking up glucose upon T-cell isolation.
Looking forward, Martin Veath, a postdoctoral researcher that works under Dr. Feske at the Department of Pathology in NYU, states "These results are timely because the field is currently exploring whether a drug class CRAC channel inhibitors can be used safely against autoimmune and inflammatory diseases in human patients, and our study fills in key details on some of the relevant mechanisms." If such a drug class was approved, treatment of viral infections would certainly improve.
-Daniel Gutierrez
Source:
https://www.sciencedaily.com/releases/2017/10/171011131649.htm
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