Reactive arthritis pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Akshun Kalia M.B.B.S.[2]
Overview
It is thought that reactive arthritis is the result of previous gastrointestinal or genitourinary infections, which results in an autoimmune condition. The most commonly associated organisms include Chlamydia, Yersinia, Salmonella, Shigella, and Campylobacter infection. It is estimated around 75% patients of reactive arthritis are positive for HLA-B27. The exact mechanism by which infecting organism cause reactive arthritis is not fully understood. It is thought that microbial antigens are similar to certain body proteins (self proteins). When an immune response is mounted against the microbial proteins, the antibodies produced against microbial proteins also reacts with the self proteins of the body causing reactive arthritis.
Pathophysiology
It is thought that reactive arthritis is the result of previous gastrointestinal or genitourinary infections, which results in an autoimmune condition. The most commonly associated organisms include Chlamydia, Yersinia, Salmonella, Shigella, and Campylobacter infection.[1][2][3]
- Reactive arthritis is associated with HLA-B27 (MHC class I molecule).
- It is estimated around 75% patients of reactive arthritis are positive for HLA-B27. Other alleles associated with reactive arthritis include HLA-B51 and HLA-DRB1.[4]
- HLA B27 association with reactive arthritis can also be attributed to the fact that patients with family history of reactive arthritis tend to have a more severe form of disease.[5]
- The exact mechanism by which infecting organism cause reactive arthritis is not fully understood. It is thought that microbial antigens are similar to certain body proteins (self proteins). When an immune response is mounted against the microbial proteins, the antibodies produced against microbial proteins also reacts with the self proteins of the body causing reactive arthritis.
- HLA-B27 incorporated MHC class I molecule presents microbial antigens to CD8 cytotoxic T cells.
- Antigen presenting cells (APCs) present microbial antigens to T helper cells which leads to their activation.
- T helper cells then differentiates into TH1 cells and TH2 cells which leads to secretion of interleukins (IL-2, IL-3, IL-4, IL-6),TNF-alpha, TGF-β and Th17 cells.
- Interleukins IL-3, IL-4, IL-6 leads to increased production of antibodies from plasma cells.
- Th17 cells release IL-17 which is also a major pro-inflammatory cytokine.[6]
- Patients with defects in T cell regulatory function may lead to more severe inflammatory process and cytokine production.[7]
- The increased cytokine and antibody production leads to destruction of microbial proteins as well as self proteins causing an autoimmune reaction.
- Furthermore, studies have shown the presence of T cells and intra-articular antibodies on synovial fluid analysis.
Reactive Arthritis in HIV patients
- Patients with HIV who later on develop reactive arthritis tend to have a more serious presentation.
- These patients present with severe generalised rash resembling psoriasis (pink color and scaly), severe arthritis and other AIDS related symptoms.
References
- ↑ Leirisalo-Repo M (2005). “Reactive arthritis”. Scand. J. Rheumatol. 34 (4): 251–9. doi:10.1080/03009740500202540. PMID 16195157.
- ↑ Braun J, Laitko S, Treharne J, Eggens U, Wu P, Distler A, Sieper J (February 1994). “Chlamydia pneumoniae–a new causative agent of reactive arthritis and undifferentiated oligoarthritis”. Ann. Rheum. Dis. 53 (2): 100–5. PMC 1005260. PMID 8129453.
- ↑ Carter JD, Hudson AP (February 2009). “Reactive arthritis: clinical aspects and medical management”. Rheum. Dis. Clin. North Am. 35 (1): 21–44. doi:10.1016/j.rdc.2009.03.010. PMID 19480995.
- ↑ Savolainen E, Kettunen A, Närvänen A, Kautiainen H, Kärkkäinen U, Luosujärvi R, Kaipiainen-Seppänen O (2009). “Prevalence of antibodies against Chlamydia trachomatis and incidence of C. trachomatis-induced reactive arthritis in an early arthritis series in Finland in 2000”. Scand. J. Rheumatol. 38 (5): 353–6. doi:10.1080/03009740902769559. PMID 19296404.
- ↑ Kaarela K, Jäntti JK, Kotaniemi KM (2009). “Similarity between chronic reactive arthritis and ankylosing spondylitis.A 32-35-year follow-up study”. Clin. Exp. Rheumatol. 27 (2): 325–8. PMID 19473576.
- ↑ Singh AK, Misra R, Aggarwal A (June 2011). “Th-17 associated cytokines in patients with reactive arthritis/undifferentiated spondyloarthropathy”. Clin. Rheumatol. 30 (6): 771–6. doi:10.1007/s10067-010-1646-5. PMID 21181220.
- ↑ Eliçabe RJ, Cargnelutti E, Serer MI, Stege PW, Valdez SR, Toscano MA, Rabinovich GA, Di Genaro MS (October 2010). “Lack of TNFR p55 results in heightened expression of IFN-γ and IL-17 during the development of reactive arthritis”. J. Immunol. 185 (7): 4485–95. doi:10.4049/jimmunol.0902245. PMID 20810989.
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