title: CD30 ligand/CD30 interaction is involved in pathogenesis of inflammatory bowel disease.
abstract: OBJECTIVE
  Although CD30 has long been recognized as an important marker in many lymphomas of diverse origin, and as an activation molecule on B and T cells, its primary function has remained obscure. Soluble CD30 (sCD30) is released from CD30 on the cell membrane by enzymatic cleavage. This study investigated the role of CD30 ligand (CD30L)/CD30 signals in intestinal mucosal damage.
  
  
  METHODS
  Serum sCD30 in patients with ulcerative colitis (UC) and Crohn's disease (CD) and healthy individuals was assessed. A model of enteritis induced by anti-CD3 monoclonal antibody injection was studied in wild-type mice and in CD30L knockout mice.
  
  
  RESULTS
  Increased sCD30 was observed in UC and CD patients, and the level was correlated with disease activity in both conditions. In a murine model of enteritis, histological intestinal damage was significantly reduced in CD30L knockout mice with decreased Th1 and Th17 cytokine levels. Moreover, blocking of CD30L/CD30 signals by CD30-immunoglobulin (CD30-Ig) resulted in reduced inflammation.
  
  
  CONCLUSIONS
  Increased sCD30 expression correlating with disease activity suggested that CD30L/CD30 signals play an important role in pathogenesis of UC and CD. CD30L/CD30 pathway acts as an accelerator of enteritis in a murine disease model. Successful blockade of enteritis by CD30-Ig suggests a potential tool for future therapy of inflammatory bowel diseases.
authors.affiliation: Department of Advanced Molecular and Cell Therapy, Kyushu University Hospital, Fukuoka, Japan. ssomada@yahoo.co.jp
authors.forename: Shinichi
authors.initials: S
authors.lastname: Somada
authors.forename: Hiromi
authors.initials: H
authors.lastname: Muta
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Nakamura
authors.forename: Xun
authors.initials: X
authors.lastname: Sun
authors.forename: Kuniomi
authors.initials: K
authors.lastname: Honda
authors.forename: Eikichi
authors.initials: E
authors.lastname: Ihara
authors.forename: Hirotada
authors.initials: H
authors.lastname: Akiho
authors.forename: Ryoichi
authors.initials: R
authors.lastname: Takayanagi
authors.forename: Yasunobu
authors.initials: Y
authors.lastname: Yoshikai
authors.forename: Eckhard R
authors.initials: ER
authors.lastname: Podack
authors.forename: Kenzaburo
authors.initials: K
authors.lastname: Tani
mesh_terms: D000328:Adult; D000818:Animals; D000911:Antibodies, Monoclonal; D017252:CD3 Complex / Q000276:immunology; D053285:CD30 Ligand / Q000097:blood*; D016022:Case-Control Studies; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000097:blood / Q000209:etiology*; D017730:Ki-1 Antigen / Q000097:blood*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D018345:Mice, Knockout; D011993:Recombinant Fusion Proteins
chemical_list: D000911:Antibodies, Monoclonal; D017252:CD3 Complex; D053285:CD30 Ligand; D017730:Ki-1 Antigen; D011993:Recombinant Fusion Proteins