A key feature of the immune system is its ability to discriminate between self and non-self. When any of the mechanisms that prevent the immune system from attacking itself break down, it can result in autoimmune disorders. Previous studies by this group have shown, in mice, that a particular type of immune T cells, known as CD8+ T cells, are essential to discriminate self from non-self.
“Until now, it wasn’t known if this mechanism exists in humans,” said Leonard Chess, M.D., also from the Division of Rheumatology at Columbia University Medical Center and a collaborating author of the study. “But our research has confirmed these CD8+ T cells do, in fact, exist in humans, and that they play an important role in stopping the immune system from attacking itself. And that understanding could lead to develop novel therapies for a wide range of autoimmune diseases.”
The Columbia researchers tested a number of patients with Type 1 diabetes, and found that the majority of them had a defect in CD8+ T cells that impacted their recognition of a common target structure known as HLA-E/Hsp60sp, previously identified by the researchers. That defect resulted in a failure of the CD8+ T cells to discriminate self from non-self.
Now that scientists have a greater understanding of the defect that leads to certain autoimmune diseases, assays could be developed to detect that defect, giving doctors an opportunity for early diagnosis, early treatment and eventually prevention of autoimmune diseases.
This scientific breakthrough could lead to a wide range of therapeutic and diagnostic possibilities, including vaccines or biotechnology agents for early diagnosis, early treatment, leading to possible cure and prevention of a variety of autoimmune diseases, including type 1 diabetes, multiple sclerosis, thyroid disease, rheumatoid arthritis, and others.
MEDICA.de; Source: Columbia University Medical Center