A new found mechanism by which a person’s immune system is dysregulated in autoimmune diabetes is described in a paper published online this week in Nature Immunology.
Leonard Harrison and colleagues found that patients with autoimmune diabetes as well as a mouse model of this disease had reduced frequencies and function of a subset of T immune cells that express a molecule called CD52. These cells were able to control the responses of other T cells responsible for causing diabetes and did so in a CD52-dependent manner. CD52 is a well-known and important target for clinical antibodies in treatment regimens, but its function in the body has hitherto been a mystery. The authors identify the receptor for CD52 as SIGLEC-10 and demonstrate its physiological function in the regulation of immune responses.
Clinical depletion of CD52 expressing cells has been used for the treatment of multiple sclerosis but can sometimes trigger other forms of autoimmune disease. These findings, demonstrating a regulatory role for CD52, might therefore offer an answer to such puzzling and unwanted side-effects.