Researchers state in JCI paper that DAF-deficient T cells lead to focal and segmental glomerulosclerosis.

A team of researchers at the University of Chicago has developed a mouse model of focal and segmental glomerulosclerosis (FSGS) that explains the link between T Cells and the disease.

It had been previously proposed that T-cell immune responses contribute to the development of some cases of FSGS, though the reason was unclear. In a study appearing in the April 1 early online table of contents for the Journal of Clinical Investigation, the investigators showed that T cells lacking the protein decay-accelerating factor (DAF) elicit an immune response that leads to this disease, which cause kidney damage.

The scientists modeled FSGS by passively transferring mouse podocyte-specific sheep antibodies into BALB/c mice with the intention of inducing Ab-dependent podocyte pathology. Mice that lacked DAF developed the hallmark features of FSGS, whereas normal mice did not.

Further testing in the mouse model led the team to conclude that DAF acts as a brake to prevent T cells from attacking podocytes. Details appear in a paper titled “Focal and segmental glomerulosclerosis induced in mice lacking decay-accelerating factor in T cells.”

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