Regulatory T cells may participate in Helicobacter pylori persistence in gastric MALT lymphoma: lessons from an animal model

• DOI: 10.18632/oncotarget.6492
• Publication Date: 2015-12-09T03:29:45Z
• Authors: Amandine Marine Laur; Pauline Floch; Lucie Chambonnier; Lucie Benejat; Victoria Korolik; Alban Giese; Pierre Dubus; Francis Mégraud; Antonio Bandeira; Philippe Lehours
• Keywords: Autoimmune Gastritis

// Amandine Marine Laur 1, 2, * , Pauline Floch Lucie Chambonnier 2 Benejat 1 Victoria Korolik 3 Alban Giese 4 Pierre Dubus Francis Mégraud Antonio Bandeira 5 Philippe Lehours University Bordeaux, Bacteriology Laboratory, France INSERM U853, Institute for Glycomics, Griffith University, Nathan QLD, Australia EA 2406, Unit Biology of Lymphocyte Populations, Immunology Department, Institut Pasteur and CIMI, Unity Treg Therapy, & Marie Curie, Paris, These authors have contributed equally to this work Correspondence to: Lehours, e-mail: [e-mail] Keywords: MALT lymphoma, regulatory T cell, animal model, Helicobacter pylori Received: August 04, 2015      Accepted: November 16, Published: December 07, 2015 ABSTRACT It has been postulated that the emergence autoimmune gastritis in neonatal thymectomised (d3Tx) BALB/c mice may be a consequence post-surgery deficit Tregs. In study, previously obtained samples from d3Tx were used order determine whether thymectomy creates cell subset thereby allowing phenomena as prerequisite GML. The splenic reserve local recruitment these cells gastric mucosa investigated using complementary molecular immunohistochemistry approaches. Higher Foxp3/CD3 ratios found spleen non-infected compared non-thymectomised (NTx) controls. results indicate relative enrichment Tregs following adult mice. absence depletion is line with auto-immune levels infiltration also stomach GML-developing versus NTx Surprisingly, inflammatory scores inversely correlated bacterial inoculum. presence small containing compartment among biopsies GML developing play role perseverance minimal numbers maintaining an antigen-dependent stimulation proliferation.