Do the insulin-producing beta cells in the pancreas unwittingly produce a signal that aids their own demise in Type 1 diabetes?
That appears to be the case, according to lipid signaling research co-led by Sasanka Ramanadham, Ph.D., professor of cell, developmental and integrative biology at the University of Alabama at Birmingham, and Charles Chalfant, Ph.D., professor of cell biology, microbiology and molecular biology, University of South Florida.
The research studied the signals that drive macrophage cells in the body to two different phenotypes of activated immune cells. The M1 type attacks infections by phagocytosis, and by the secretion of signals that increase inflammation and molecules that kill microbes. The M2 type acts to resolve inflammation and repair damaged tissues.
Autoimmune diseases result from sustained inflammation, where immune cells attack one’s own body. In Type 1 diabetes, macrophages and T cells infiltrate the pancreas and attack beta cells. As they die, insulin production drops or vanishes.
UAB researcher Ramanadham has spent decades studying lipid signaling in Type 1 diabetes. At South Florida, Chalfant studies lipid signaling in cancer, and his lab provides mass spectrometry expertise for both studies. Mass spectrometry is a very sensitive approach to identify different classes of lipids and quantify the abundances of such lipids.
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