Reactive arthritis

Reactive arthritis, formerly known as Reiter’s syndrome, is inflammation of a joint which usually develops after an infection, and that infection is typically a sexually transmitted disease or gastroenteritis. Reactive arthritis is part of a group of diseases called seronegative spondyloarthropathies. Spondyloarthropathies are autoimmune, inflammatory joint diseases, and they’re seronegative, which refers to the fact that an auto-antibody called rheumatoid factor is absent from the blood.

Normally, the immune cells are ready to spot and destroy anything foreign that could cause the body harm. To help with this, most cells in the body have a set of proteins that combine together to form something called a major histocompatibility complex, or MHC, and this is a molecule that sits on the surface of their cell membrane. There are two kinds of MHC molecules, class I and class II. Class I molecules are found on most cells in the body, and they present molecules from within the cell for the immune system to continually sample. Normally the molecule’s just a sample from inside the cell, also known as a self-antigen. When immune cells pass by, they recognize this self-antigen as harmless so there’s no response.

MHC class II molecules are found specifically on phagocytic cells like macrophages which destroy and digest foreign pathogens like bacteria. Once a macrophage destroys a bacterium, it presents a piece of that bacterium on its MHC class II receptor, and the macrophage then makes its way to the lymph node to find some T-lymphocytes. A type of T-lymphocyte, called a CD4+ T-cell, also known as a helper T-cell, uses its T-cell receptors to bind to the foreign antigen presented by the MHC class II molecule. If the helper T-cell binds strongly, the antigen is recognized as foreign, and the helper T-cell switches on the corresponding B-cell, so it can start producing a whole lot of antibodies. These antibodies bind to the specific pathogen, and typically prevent it from attacking the host’s cells and, at the same time, they “tag” the pathogen for further destruction by other immune cells.

Reactive arthritis can develop after a sexually transmitted infection like chlamydia, or after gastroenteritis caused by bacteria like salmonella, shigella, yersinia, campylobacter, and E.coli. These bacteria are all gram negative, so they have molecules on their outer surface called lipopolysaccharides, sometimes shortened to LPS. These molecules produce a strong immune response, so much so, that their other name is endotoxin. Also, most individuals with reactive arthritis have the specific gene HLA-B27 which is one of many genes that has code to make MHC class I receptors. HLA-B27 is also associated with other inflammatory diseases like psoriasis and ankylosing spondylitis. Exactly how reactive arthritis develops, though, is still unclear, but it probably has something to do with the way that lipopolysaccharides react with the MHC molecules on a cell surface.

Because the immune system takes a while to present foreign antigens and kick T-cells into gear, reactive arthritis often starts two to three weeks after an initial infection. Tissues usually targeted by the immune system are tissues of the joint spaces, but occasionally, the immune system also attacks tissues like the lining of the urethra and the conjunctiva. In fact, when all three of these tissues are affected, meaning the joint spaces, the urethra, and the conjunctivae, that causes a triad which associates arthritis, urethritis and conjunctivitis. However, this triad is very uncommon, and usually only the joint spaces are affected. Other tissues that are sometimes involved include the cervix in women and the pericardium of the heart.