A study published in Human Immunology has described, for the first time, a link between an immunosuppressive protein on the surface of T cells and the development of systemic lupus erythematosus, or SLE. This protein, human leukocyte antigen G (HLA-G), is expressed on fetal derived placental cells and is thought to play a role in immune tolerance during pregnancy.
HLA-G has been the subject of intense study in the last two decades. In particular, scientists have been interested in how HLA-G-mediated pathways affect rejection after organ transplantation, or how tumors suppress hijack these to evade immune detection.
Now, the research team led by Francesco Puppo at the University of Genoa has identified that patients with SLE have significantly elevated levels of HLA-G. The protein was found on the membrane of peripheral blood mononuclear cells, a subset of white blood cells that includes T cells and monocytes. The significant difference in HLA-G levels between lupus patients and healthy controls points to the protein’s possible involvement in the onset or progression of this autoimmune disease.
SLE affects nearly every organ system from the skin, joints and central nervous system to the brain and kidneys. The disease is more prevalent in women than men and is thought to be a result of complex genetic, environmental and hormonal factors. Lupus is characterized by an exaggerated immune response to the body’s own cells and tissues, causing this widespread organ damage.
Based on their findings, the authors hypothesize that the increased production of HLA-G on the surface of immune cells could reflect an attempt to control the imbalanced immune responses occurring during the systemic autoimmune diseases.
Further clinical studies are due to establish whether HLA-G could be leveraged for diagnostic or therapeutic purposes.