03:05pm Thursday 14 December 2017

Yale Researchers Find A Surprising Culprit in Lupus

The findings, reported in the December 16 issue of the journal Immunity, focused on the role the dendritic cell plays in systemic lupus erythematosus or SLE, a chronic inflammatory disease that affects a variety of parts of the body including skin, joints, blood and kidneys. Dendritic cells are important for initiating the immune response to pathogens but it is unclear what role they play in autoimmune diseases, such as SLE.

The immunoflourescent image shows T cells (green) and dendritic cells (blue) and dividing immune system cells (red) active in a diseased kidney. This illustrates how dendritic cells are active locally along with T cells in the autoimmune disease lupus.

A team led by Mark Shlomchik, Professor of Laboratory Medicine and of Immunobiology and senior author of the paper, knocked out dendritic cells in lupus-prone mice and found a dramatic reduction in symptoms of lupus. They also discovered another surprise.

Dendritic cells were believed to be crucial in activating T cells, which along with B cells comprise the two main arms of the immune system. However, knocking out the dendritic cells in lupus mice did not reduce the activation of pathogenic T cells as expected. Instead, the cells disappeared from inflamed tissue such as kidneys, causing a reduction in symptoms in lupus mice lacking the dendritic cells. Dendritic cells appear to play a localized role in lupus tissue damage and so might make a good therapeutic target for lupus and possibly other autoimmune diseases as well, the authors say.

“Dendritic cells could be having the same effects in a variety of other autoimmune diseases, but we will not know until we do similar experiments in other disease models,” Shlomchik said.

Other Yale authors of the paper are Lino Teichmann, Michael Kashgarian, and Michelle Harris-Ols.

The work was funded by the National Institute of Arthritis and Musculoskeletal Diseases and the Lupus Research Institute.

PRESS CONTACT: Bill Hathaway 203-432-1322


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