title: Expression of T-cell immunoglobulin- and mucin-domain-containing molecules-1 and -3 (Tim-1 and Tim-3) in Helicobacter pylori infection.
abstract: BACKGROUND
  Th immune response plays an important role in Helicobacter pylori (H. pylori) infection. Tim-1 and Tim-3 are expressed on terminally differentiated Th2 and Th1 cells, respectively, and participate in the regulation of Th immune response. Until now, the role of Tim in H. pylori infection remains unclear.
  
  
  METHODS
  (1) Lymphocytes isolated from the spleen of BALB/c mice were co-cultured with different concentrations of viable H. pylori. Alternatively, mice were challenged by viable H. pylori to set up the H. pylori infection model. (2) The expression of Tim-1 and Tim-3 on mRNA level in lymphocytes or spleen of mice was determined by RT-PCR. The percentage of Tim-3-positive cells was determined by flow cytometric analysis. The production of cytokine in supernatants was measured by standard sandwich cytokine ELISA.
  
  
  RESULTS
  (1) Co-culture: At 12 hours, there was markedly decreased production of Tim-1 and increased production of Tim-3 in lymphocytes co-cultured with H. pylori compared with normal control. The change of Th2 cytokine had the similar tendency as that of Tim-1 expression; alternatively, the change of Th1 cytokine had the similar tendency as that of Tim-3 expression. (2) INFECTION: Tim-1 expression was declined in infected mice compared with control group; in the contrast, Tim-3 expression was increased. Furthermore, the expression of Tim-1 and Tim-3 mRNA in spleen was significantly positively correlated with the level of Th2 and Th1 cytokine in gastric homogenized supernatant, respectively.
  
  
  CONCLUSIONS
  H. pylori could inhibit the differentiation of T lymphocytes toward Th2 cells, promote the Th1 cell differentiation, and induce Th1-biased immune response. The expression of Tim-1 and Tim-3 could reflect Th2 and Th1 immune response, respectively, which provide evidence for the prevention and treatment of H. pylori infection and correlation diseases through regulation of Tim-1 and Tim-3.
authors.affiliation: Institute of Digestive Diseases, the First Affiliated Hospital of Nanchang University, China.
authors.forename: Sijun
authors.initials: S
authors.lastname: Hu
authors.forename: Yong
authors.initials: Y
authors.lastname: Xie
authors.forename: Nanjin
authors.initials: N
authors.lastname: Zhou
authors.forename: Lei
authors.initials: L
authors.lastname: Jin
authors.forename: Yan
authors.initials: Y
authors.lastname: Tan
authors.forename: Dongsheng
authors.initials: D
authors.lastname: Liu
authors.forename: Yanfeng
authors.initials: Y
authors.lastname: Gong
authors.forename: Li
authors.initials: L
authors.lastname: Liu
authors.forename: Jinlin
authors.initials: J
authors.lastname: Liu
authors.forename: Wei
authors.initials: W
authors.lastname: Liu
authors.forename: Yanxia
authors.initials: Y
authors.lastname: Chen
authors.forename: Yuting
authors.initials: Y
authors.lastname: Zhang
authors.forename: Nonghua
authors.initials: N
authors.lastname: Lv
mesh_terms: D000818:Animals; D002454:Cell Differentiation; D018920:Coculture Techniques; D016207:Cytokines / Q000378:metabolism; D005753:Gastric Mucosa / Q000378:metabolism; D016481:Helicobacter Infections / Q000276:immunology*; D000072596:Hepatitis A Virus Cellular Receptor 1; D000072597:Hepatitis A Virus Cellular Receptor 2; D008565:Membrane Proteins / Q000378:metabolism*; D051379:Mice; D008807:Mice, Inbred BALB C; D012333:RNA, Messenger / Q000378:metabolism; D011991:Receptors, Virus / Q000378:metabolism*; D013154:Spleen / Q000166:cytology; D018417:Th1 Cells / Q000276:immunology / Q000382:microbiology; D018418:Th2 Cells / Q000276:immunology / Q000382:microbiology
chemical_list: D016207:Cytokines; C442240:Havcr1 protein, mouse; C442241:Havcr2 protein, mouse; D000072596:Hepatitis A Virus Cellular Receptor 1; D000072597:Hepatitis A Virus Cellular Receptor 2; D008565:Membrane Proteins; D012333:RNA, Messenger; D011991:Receptors, Virus