Pathogenesis of a postenteritic reactive arthritis

Current theory for the pathogenesis of a postenteritic reactive arthritis

Bacterial lipopolysaccharide antigens (but not viable organisms or nucleotides) from the pathogens ( Yersinia, Shigella, Salmonella ) causing the infectious gastroenteritis have been shown to be deposited in the joints of patients who develop a postenteritic reactive arthritis. These bacterial cell wall components are thought to incite inflammation in the joint. The role that HLA-B27 plays in the pathogenesis is debated. One possibility is that recirculating HLA-B27 –restricted T cells present bacteria-derived peptides with arthritogenic properties to the immune system in a unique way, leading to inflammation. Another postulate is that there is molecular mimicry between the HLA-B27 molecule and the bacterial antigens, causing an aberrant immune response leading to altered or defective intracellular killing by HLA-B27 –positive cells, resulting in persistence of arthritogenic pathogens. A third hypothesis relates to the tendency for the HLA-B27 heavy chain to misfold when the cell is under stress. This results in heavy chains accumulating in the endoplasmic reticulum leading to an “unfolded protein response,” causing the release of inflammatory cytokines. The chronic persistence of bacterial antigens may stress the HLA-B27 –positive cells, leading to B27 heavy chain misfolding and the unfolded protein response. However, because HLA-B27 positivity is neither necessary nor sufficient to cause reactive arthritis, additional genetic (endoplasmic reticulum aminopeptidase–1 and interleukin 23R polymorphisms) and environmental factors likely play a role in the pathogenesis of postenteritic reactive arthritis.


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