Regulatory T Cell Deficient Mice Develop Lupus-Like Disease
A new study showed that mice deficient in regulatory T cells develop systemic autoimmune disease similar to lupus. The study entitled “Regulatory T cell deficient scurfy mice develop systemic autoimmune features resembling lupus-like disease” was published in Arthritis Research & Therapy.
Scurfy mice do not have regulatory T cells (Treg), crucial to suppress autoimmune diseases, and develop a severe and generalized autoimmune condition culminating in death at young age. These mice show some features that are similar to those found in systemic lupus erythematosus (SLE). SLE is an autoimmune disease that can affect several parts of the body, including the skin, joints, heart, lungs, blood, kidneys, and brain. In an autoimmune disease the immune system cannot distinguish between foreign substances and its own cells and tissues. As a result, the immune system generates antibodies directed against its own cells and tissues, called “auto-antibodies” causing inflammation, pain, and damage in various parts of the body. It has been observed that active SLE is associated with lower Treg numbers and reduced Treg function, but direct role of Treg disfunction in the pathogenesis of lupus-like manifestations has still not been described.
In this study, the research team characterized the multi-organ pathology, autoantibody profile and blood count alterations in scurfy mice and found similarities to lupus-like disease. They found that scurfy naturally develop severe lung inflammation and hematological alterations similar to those observed in SLE, as previously shown. Moreover, these mice demonstrated additional features of SLE such as severe dermatitis and arthritis. The authors transferred CD4 T cells from scurfy to C57BL/6/nude mice which do not have T cells, and observed the induction of production of auto-antibodies and inflammation of lung, skin and kidneys.
The authors do not consider scurfy mice as an experimental model of lupus since these mice show more autoimmune features than typical for SLE. These findings do, however, favor the hypothesis that lack of Treg function and the consequent loss of peripheral tolerance leads to systemic autoimmune features similar to the ones observed in SLE.
