P397 Analysis of Mucosal TNFSF15/TL1A Expression in Korean IBD Patients
C.S. Eun*1, D.S. Han1, A.R. Lee1, J.H. Pyo2, Y.H. Oh2
1Hanyang University Guri Hospital, Gastroenterology, Guri, Korea, Republic of, 2Hanyang University Guri Hospital, Pathology, Guri, Korea, Republic of
It has been well known that genetic mutations and the epidemiology of inflammatory bowel disease (IBD) differ between Asia and the West. However, TNF superfamily member 15 (TNFSF15) gene has been identified as a common susceptibility gene in Asian and Western IBD patients, suggesting that TNFSF15 may play an important role in the pathogenesis of IBD. TNFSF15/TNF-like cytokine 1A (TL1A) is a proinflammatory cytokine and a member of the TNF α superfamily, mainly expressed on activated T cells. We investigated mucosal TL1A expression by immunohistochemistry (IHC) in Korean IBD patients.
TL1A expression was investigated in resected ileal specimens from 8 Crohn's disease (CD) patients and 8 non-IBD controls by IHC using an affinity-purified mAb against TL1A. TL1A expression was also studied in endoscopically biopsied colonic specimens from 8 ulcerative colitis patients and 8 non-IBD controls. In addition, the mucosal expressions of CD3, CD4, and CD8, T cell markers, were examined in ileal and colonic specimens of IBD patients and non-IBD controls.
The expression of TL1A at the protein level was absent or minimal in ileal and colonic tissues from controls. On the contrary, intense expression of TL1A was identified in ileal and colonic specimens from IBD patients, especially in CD patients. Staining for TL1A was significantly increased in inflammed area of ileal tissues compared to non-inflammed area from CD patients. CD3, CD4, and CD8 expressions were also significantly increased in ileal and colonic specimens from IBD patients compared to those from controls.
Mucosal TL1A is upregulated in IBD patients, suggesting an important role of TL1A in the pathogenesis of IBD. Further functional studies of TL1A will provide a better understanding of the pathogenesis of IBD.