Study Unveils New Therapeutic Target To Suppress Autoimmune Inflammation Caused By Loss Of Regulatory T Cell Function – Zoo House News

Study Unveils New Therapeutic Target To Suppress Autoimmune Inflammation Caused By Loss Of Regulatory T Cell Function – Zoo House News

  • Science
  • January 25, 2023
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New research details how self-reactive T cells – white blood cells that mistakenly attack healthy instead of infected cells, thereby triggering an autoimmune or inflammatory response – are kept in check by regulatory T cells.

Regulatory T cells, or Tregs, are patrolling white blood cells that help maintain law and order among the body’s sometimes overzealous disease-fighting T cells, also known as CD4 effector cells, or Teffs.

New research details how self-reactive T cells – white blood cells that mistakenly attack healthy instead of infected cells, thereby triggering an autoimmune or inflammatory response – are kept in check by regulatory T cells. the researchers found.

This rapid Treg intervention reduces the size and number of Teff cells to appropriately control the magnitude of the immune response. However, when Tregs become depleted or lose function, problems can arise with the now unmanaged population of Teffs, which can cause disease by becoming self-reactive or hyper-inflammatory.

The latest information on how Tregs work to suppress activated teff cells suggests that drug therapies could be used in cases where Tregs aren’t working properly.

Research into the strategies used by Tregs to control teff cell populations was recently conducted in the immunology labs of Ram Savan, associate professor of immunology at the University of Washington School of Medicine, and Steven F. Ziegler of the Benaroya Research Institute in Seattle . The main authors were Lomon So and Kazushige Obata-Ninomiya.

Her team used a new technique called SPEED to detect changes in teff protein production that could not be detected using traditional methods

Their findings were published in the Journal of Experimental Medicine.

The scientists explained that the thymus gland, where T cells develop, normally recognizes and filters out self-reactive T cells. However, since this is not a perfect process, some self-reactive T-cells escape elsewhere in the body. If not suppressed, they have the potential to multiply and cause autoimmune and inflammatory diseases.

In healthy people, cell signaling pathways increase when teffs are activated by the presence of pathogens. These signals coordinate the growth and proliferation of white blood cells to fight off the invading pathogen and keep the host healthy.

As a countermeasure to ensure that teffs do not cause rampant inflammation or autoimmunity, Tregs produce a combination of two cytokines, interleukin 10 (IL-10) and translational growth factor beta (TGFb), to increase mTORC1 signaling in activated teff cells interrupt. This blockade in turn inhibits the translation of certain messenger RNAs. Translation is a cellular activity in which mRNA is decoded into a series of amino acids to form proteins.

Tregs repress the translation of messenger RNAs that contain a specific motif. When these messenger RNAs are blocked, the teff cell has trouble making fresh proteins. Therefore, by actively controlling messenger RNA translation in Teff cells, Treg cells can shut down the protein machinery that was preparing to go into overdrive. Tregs thereby deactivate the stimulated Teff cells to manage the inflammatory response and keep it within reasonable limits.

‘This is a highly efficient regulatory mode: inhibiting the ramp-up of biosynthesis that drives cell division,’ the scientists stated. “It stops the spread before it starts.” It is also a novel way to induce and maintain immune tolerance to avoid an autoimmune response.

When the body experiences an acute loss of regulatory T cells, teff cells exhibit a rapid and aberrant increase in protein synthesis in an effort to replenish their protein biomass in preparation for cell division.

In this case, the researchers learned that they could directly suppress protein synthesis in teff cells by using a small molecule inhibitor called rocaglamide A or RocA. This chemical was first isolated in China in 1982 from a plant called Greater Aglaia. The chemical has already been shown by several other laboratories to have a variety of anti-insect, anti-fungal and anti-cancer properties.

The experiments conducted in Savan and Ziegler’s labs suggest that RocA may also have other therapeutic benefits, the researchers noted, by mitigating the unwanted inflammatory response that occurs by activating CD4-Teff cells. Like Treg cells, the chemical RocA repressed protein synthesis by controlling RNA translation.

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