Researchers performed studies on mice that were engineered to lack the protein found on the surface of T cells, called P-selectin glycoprotein ligand-1. PSGL-1 acts as a negative regulator of T cell function, according to scientist Linda Bradley, PhD.
“PSGL-1 has the broad capacity to dampen T cell signals and promote the exhaustion of T cells in viral and tumor mouse models,” Dr. Bradley explained.
The researchers discovered that when PSGL-1 was missing, T cells could remain active longer than they would normally, allowing the mice to completely eliminate lymphocytic choriomeningitis virus infections, which could typically last months.
“Blocking PSGL-1 may enhance the immune response to cancer and chronic viral infections such as hepatitis,” said Dr. Bradley. “In contrast, activating PSGL-1 may be a way to inhibit immune responses that could potentially be used to treat autoimmune diseases, such as rheumatoid arthritis, psoriasis, multiple sclerosis and lupus.”
The discovery may help create new ways to regulate T cell responses to clinical infections, autoimmune diseases and tumors that don’t response to existing treatments.
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