The local and systemic T-cell response to Helicobacter pylori in gastric cancer patients is characterised by production of interleukin-10 B. Samuel Lundin a, ⁎ , Karin Enarsson a , Bert Kindlund a , Anna Lundgren a , Erik Johnsson b , Marianne Quiding-Järbrink a , Ann-Mari Svennerholm a a Department of Microbiology and Immunology, Institute of Biomedicine, Göteborg University Vaccine Research Institute (GUVAX) and Mucosal Immunobiology and Vaccine Center (MIVAC), Göteborg University, Box 435, 40530 Göteborg, Sweden b Department of Surgery, Göteborg University, Göteborg, Sweden Received 20 March 2006; accepted with revision 26 July 2007 Available online 10 September 2007 Abstract Helicobacter pylori causes a life-long infection that may lead to development of gastric adenocarcinoma (GC) and thereby cause major worldwide health problems. The present study was designed to study whether those that develop GC have an altered immune response to H. pylori compared to individuals that remain asymptomatic. When stimulated with H. pylori antigens, T cells from both peripheral blood and gastric mucosa of H. pylori-infected GC patients produced high amounts of IL-10, while the IL-10 production from blood T cells of H. pylori- infected asymptomatic subjects was low. Furthermore, mRNA levels of IL-10 were increased in the gastric mucosa of GC patients. In addition, the frequency of activated CD8 + T cells was markedly reduced in stomach mucosa of patients with GC compared to asymptomatic individuals. We propose that the increased production of the suppressive cytokine IL-10 in H. pylori-infected GC patients leads to a diminished cytotoxic anti-tumour T-cell response in the stomach, which may contribute to tumour progression in subjects suffering from GC. © 2007 Elsevier Inc. All rights reserved. KEYWORDS Helicobacter pylori; Gastric adenocarcinoma; T-cell; Interleukin-10; Human Introduction Helicobacter pylori is a gram-negative bacterium that colonises the human gastric and duodenal mucosa, and causes a life-long infection. The majority of infected indi- viduals remain asymptomatic, but 10–15% of those infected develop peptic ulcers, and in a few percent of the individuals the infection leads to development of non-cardia gastric adenocarcinoma (GC) [1]. GC is the second most common cause of cancer death in the world [2], and it has been estimated that more than half of the non-cardia GC are caused by H. pylori infection [3]. The mechanisms leading to development of GC in infected individuals are presently unclear. In general, the development of a tumour is the result of altered cell growth regulation as well as failure of the host to induce a sufficient immunological anti-tumour response. In the H. pylori-infected stomach, it is feasible ⁎ Corresponding author. Fax: +46 31 7736205. E-mail address: samuel.lundin@microbio.gu.se (B.S. Lundin). 1521-6616/$ - see front matter © 2007 Elsevier Inc. All rights reserved. doi:10.1016/j.clim.2007.07.011 available at www.sciencedirect.com www.elsevier.com/locate/yclim Clinical Immunology (2007) 125, 205–213