Pro-inflammatory cytokines (tumor necrosis factor, interferon ϒ, interleukin-1β, IL-6 and IL-17) promote autoimmune inflammation and tissue damage, while anti-inflammatory cytokines help resolve inflammation and facilitate tissue repair. (Kim and Moudgil 2017) Macrophages, monocytes and CD4+ T helper cells (Th1) produce tumor necrosis factor, which is a key driver of inflammation.
This aspect of inflammation is a general feature of rheumatoid arthritis (RA). RA is characterized by chronic inflammation of the synovial tissue, joint dysfunction and tissue damage in the joints. A major mechanism of autoimmune disorders is an altered balance between the pathogenic T helper 17 (Th17) and protective T regulatory (Treg) cells. A shift towards Th17 promotes inflammation, neutrophil influx, induction of TNFα and joint damage in the case of rheumatoid arthritis. A shift towards Treg control promotes an anti-inflammatory tone. Perturbation of this balance can facilitate the induction and progression of autoimmune pathology.(Moudgil 2015). A short video link describes autoimmune diseases (“friendly-fire”) and pharmacological approaches for treatment. (AARDA 2014)
When the immune system attacks host tissue, the results can be devastating. There are many types of tissues and organs that can be impacted by autoimmune attack. The autoimmune attack can destroy the affected tissue and also negatively impact organ function.(Help 2017)
Defective inflammation resolution is an underlying cause of prevalent chronic inflammatory diseases, such as atherosclerosis.(Viola and Soehnlein 2015) Put another way, chronic inflammation is a failure to resolve inflammatory mediators leading to a chronic state of dysregulation. Resolvins involved in the acute phase of inflammation support resolution responses and return to homeostasis. Importantly, proresolution pathways are not immunosuppressive. Dysregulation in resolving inflammation may be due to enzymatic insufficiency of the enzymes involved in converting long chain fatty acid metabolites to their oxidized derivatives that form the superfamily of pro-resolving mediators.(Fredman and Tabas 2017)