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The immune system’s main players — the B cells and T cells, as well as others — are credited for helping the body ward off invaders. And rightly so. But to work their magic, they rely on under-recognized calcium channels, gates in the cell surface that, among other actions, switch the immune cells into “action” mode.
Many unknowns remain about how these cells function, but Richard Lewis, PhD, professor of molecular and cellular physiology, is working to close the gaps in knowledge. He explains in the video above:
We’re mostly interested in two things related to these channels: First, we would like to understand how these channels work. How is it that contact with the antigen-presenting cell turns these cells on to admit calcium into the T cell?
A second area of interest is to understand what happens when the calcium comes into the cell.
Malfunctions in these channels can lead to severe immunodeficiencies or other problems, Lewis says:
We may be able to design better drugs in the future that target these channels to either inhibit them, which would be useful therapy for treating autoimmune disorders like arthritis, multiple sclerosis and lupus, or to potentiate the activity of these channels, which would be a useful way of boosting the immune response in patients with immunosuppressed conditions.
Learn more about Stanford Medicine’s Biomedical Innovation Initiative and about other faculty leaders who are driving biomedical innovation here.
Previously: ‘Pacemaker’ channels in hair stem cells offer clues to tissue regeneration, say Stanford experts, Found: A molecule mediating memory meltdown in aging immune systems and Women and men’s immune system genes operate differently, Stanford study shows