New research shows bystander cell accumulation may play an active role in countering autoimmune diseases and curbing inflammation.
Autoimmune diseases are those in which the immune system attacks the body’s own cells leading to inflammation and damage of organs and tissues. Type 1 diabetes (T1D) is an example of an autoimmune disease caused by destruction of insulin-producing pancreatic cells (islet beta cells) by the immune system. Cytotoxic T cells that recognize islet beta cell antigens are the main immune cells responsible for the changes seen in T1D, but cytotoxic T cells that do not recognize these antigens are also found to infiltrate the pancreatic tissue. These cells have been designated bystander cells and have been thought to passively contribute to autoimmune-related tissue damage.
T regulatory cells (Tregs) have been considered the primary immune cell type that reduces the autoimmune process, but bystander cells have recently been shown to counteract, not enhance, the inflammatory actions of antigen-specific cytotoxic T cells. To better understand the anti-inflammatory role of bystander cells in autoimmune disease, researchers conducted a study using a laboratory mice model of T1D. Essentially, they transferred various levels of antigen-specific and bystander cells to these mice and determined the effects on pancreatic cell survival with the use of confocal microscopy.
Mice that received lower levels of bystander cells when compared to antigen-specific cytotoxic T cells had more beta cell damage and hyperglycemia (indicative of a diabetic state). In contrast, mice that received equivalent levels of antigen-specific T cells and bystander cells had significantly lower levels of beta cell damage. Diabetes did not develop in mice with high levels of bystander cells, and there was less activation of the antigen-specific cytotoxic T cells and inflammation. Furthermore, the anti-inflammatory function of the bystander cells is not related to the expansion of Treg cells.
Bystander cells were found to specifically and efficiently concentrate in the islets of the T1D mouse models. The presence of high levels of bystander cells in the islets led to a reduction of autoimmune response by antigen-specific cytotoxic T cells, leading to a significant decrease in cell and tissue damage. This new insight provides information that can be harnessed to develop novel immune-based treatments for T1D.
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Bystander T cells can steal the show in resolving inflammation: Researchers show that non-specific bystander T cells can play an active role in countering type 1 diabetes. (2018). ScienceDaily. Retrieved 23 April 2018, from https://www.sciencedaily.com/releases/2018/03/180323141342.htm