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Posted on Jun 10, 2018, 5 p.m.
Cellular network involved in initiating and maintaining rheumatoid arthritis has been identified by researchers from Osaka University, it is suggested the network can be targeted using novel immunotherapeutic approaches to reduce joint inflammation, as published in the journal Immunity.
Action of various cytokines that are produced by the immune system are involved in chronic inflammation disorders such as rheumatoid arthritis, one cytokine is IL-17 produced by TH17 cells. TH17 cells are known for playing roles in autoimmune diseases, but it is unclear how they control other inflammatory cells.
Using model mice researchers found how TH17 cells interact with other cells at inflammation site to influence the production of inflammatory cytokine molecules, and have shown inflammatory cytokine GM-CSF is critical for development of arthritis in mice.
GM-CSF produced by T cells and stromal cells in connective tissue was found to contribute to joint inflammation in the animals, only stromal cell derived GM-CSF was required to initiate arthritis.
GM-CSF was secreted by stromal cells in response to stimulation for IL-17 from inflammatory TH17 cells. GM-CSF is secreted by a group of innate immune cells involved in nonspecific defense mechanisms, cells increase in number within inflamed joints in response to production of IL-17 by TH17 cells and other inflammatory cytokines, which contribute to development and maintenance of rheumatoid arthritis within the animals. When cells that produce GM-CSF were removed from joint lining significant reduction in severity of arthritis was observed.
According to the researchers findings demonstrate developing novel immunotherapeutic approaches that target this cellular network to reduce chronic joint inflammation would be advantageous.
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