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Tropomyosins in human diseases: ulcerative colitis
1Division of Gastroenterology and Hepatology, Department of Medicine, Crohn's and Colitis Center of New Jersey, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, NJ 08903, USA. daskm@umdnj.edu
Advances in Experimental Medicine and Biology
|February 13, 2009
Summary
Autoimmune responses targeting tropomyosin (Tm) are key in ulcerative colitis (UC) pathogenesis. Specifically, hTm5 protein on colon cells triggers immune responses and autoantibodies, leading to colon damage in UC patients.
Area of Science:
- Immunology
- Gastroenterology
- Cell Biology
Background:
- Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD) with complex etiology, involving genetic, environmental, and immune factors.
- Autoimmune responses against cytoskeletal proteins, particularly tropomyosin (Tm), are implicated in UC pathogenesis.
- The colonic epithelial Tm isoform, hTm5, is a potential autoantigen in UC.
Purpose of the Study:
- To investigate the role of hTm5 and its interaction with colon epithelial protein (CEP) in UC pathogenesis.
- To determine if anti-hTm5 autoantibodies are pathogenic in UC.
Main Methods:
- Analysis of hTm5 and CEP expression in UC mucosa.
- Assessment of immune responses (B-cell and T-cell) to hTm5 in UC patients.
- Detection of autoantibodies against hTm5 in circulation and colon tissue.
- Evaluation of the pathogenic potential of anti-hTm5 autoantibodies.
Main Results:
- hTm5 is expressed on the colon epithelial cell surface, facilitated by CEP, and both are increased with pro-inflammatory cytokines like gamma-interferon.
- hTm5 expression is significantly elevated in UC mucosa compared to normal tissue.
- UC patients exhibit humoral and cellular immune responses to hTm5, not observed in healthy or control subjects (Crohn's disease, lupus).
- Pathogenic autoantibodies against hTm5 are present in UC patients' circulation and colon mucosa, causing epithelial cell destruction via antibody and complement-mediated cytolysis.
Conclusions:
- hTm5, presented on the colon epithelial surface via CEP, is a critical autoantigen in UC.
- Autoimmune responses and pathogenic autoantibodies against hTm5 contribute significantly to colon epithelial cell destruction in UC.
- Targeting the hTm5-mediated autoimmune pathway may offer novel therapeutic strategies for UC.
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