Reactive arthritis is triggered by an infection, either of the genitourinary or gastrointestinal tracts; the common triggering bacteria in enteric ReA include salmonella, shigella, yersinia, and campylobacter. It is still not clear how such different bacteria can lead to a similar clinical picture and have a similar association with the MHC class I antigen HLA-B27. Common both to enterogenic and urogenic bacteria is the type of peripheral joint involvement. However, this is not so different from other bacteria-associated arthritides and is probably the consequence of bacteria persistent inside the joint. What is unique to these bacteria is the HLA-B27-association and the nearly exclusively B27-linked clinical manifestations as sacroiliitis and iritis. Shigella-induced ReA has the highest B27-association while in salmonella- and chlamydia-induced ReA a lower association can be found. Mucosal entry of enterogenic bacteria give easy access to macrophages which might be important for the transport into the joint. Although bacteria-specific antibodies are of diagnostic value, the humoral immune response does not explain the immunopathogenesis and MHC-association of this disease. Bacteria-specific T-cells have been constantly found in the synovial fluid from ReA patients and have been further analysed. The identification of immunodominant antigens of these bacteria is of great importance to understand the pathogenesis. Although an antigen shared by all bacteria has not been identified until now progress is being made in this field. We have also to consider the possibility that these bacteria are not only driving the immune response themselves but rather work as a trigger for autoimmunity.