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

Autor: Laur, Amandine Marine, Floch, Pauline, Chambonnier, Lucie, Benejat, Lucie, Korolik, Victoria, Giese, Alban, Dubus, Pierre, Mégraud, Francis, Bandeira, Antonio, Lehours, Philippe
Přispěvatelé: Infection à helicobacter, inflammation et cancer, Université Bordeaux Segalen - Bordeaux 2-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire de bactériologie, CHU Bordeaux [Bordeaux], insitute for glycomics, Griffith University [Brisbane], Histologie et Pathologie Moléculaire, Université Bordeaux Segalen - Bordeaux 2, Biologie des Populations Lymphocytaires, Centre National de la Recherche Scientifique (CNRS)-Institut Pasteur [Paris], Alban Giese and the Experimental Histology unit were funded by the Cancéropôle Grand Sud Ouest, Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS)
Jazyk: angličtina
Rok vydání: 2016
Předmět:
regulatory T cell
Real-Time Polymerase Chain Reaction
T-Lymphocytes
Regulatory

Helicobacter Infections
Immunoenzyme Techniques
Mice
MESH: Lymphoma
Non-Hodgkin

Stomach Neoplasms
MESH: Reverse Transcriptase Polymerase Chain Reaction
Animals
MESH: Animals
RNA
Messenger

MALT lymphoma
MESH: Immunoenzyme Techniques
MESH: Lymphoma
B-Cell
Marginal Zone

MESH: Mice
MESH: RNA
Messenger

Helicobacter pylori
Reverse Transcriptase Polymerase Chain Reaction
MESH: Real-Time Polymerase Chain Reaction
Lymphoma
Non-Hodgkin

animal model
MESH: Helicobacter Infections
MESH: T-Lymphocytes
Regulatory

Lymphoma
B-Cell
Marginal Zone

MESH: Stomach Neoplasms
Disease Models
Animal

MESH: Gastric Mucosa
Gastric Mucosa
MESH: Helicobacter pylori
[SDV.IMM]Life Sciences [q-bio]/Immunology
MESH: Disease Models
Animal

Research Paper
Zdroj: Oncotarget
Oncotarget, Impact journals, 2016, pp.3394-402. ⟨10.18632/oncotarget.6492⟩
Oncotarget, 2016, pp.3394-402. ⟨10.18632/oncotarget.6492⟩
ISSN: 1949-2553
DOI: 10.18632/oncotarget.6492⟩
Popis: International audience; It has been postulated that the emergence of autoimmune gastritis in neonatal thymectomised (d3Tx) BALB/c mice may be a consequence of post-surgery deficit in Tregs. In this study, previously obtained samples from d3Tx mice were used in order to determine whether thymectomy creates a deficit in this T cell subset thereby allowing the emergence of autoimmune phenomena as a prerequisite for GML. The splenic Treg reserve and the local recruitment of these cells in the gastric mucosa were investigated using complementary molecular and immunohistochemistry approaches. Higher Foxp3/CD3 ratios were found in the spleen of non-infected d3Tx mice compared to non-thymectomised (NTx) controls. These results indicate a relative enrichment of Tregs following thymectomy in adult mice. The absence of Treg depletion in d3Tx mice is in line with the absence of auto-immune gastritis in non-infected d3Tx mice. Higher levels of T cell and Treg infiltration were also found in the stomach of GML-developing d3Tx mice versus NTx mice. Surprisingly, inflammatory scores inversely correlated with the bacterial inoculum. The presence of a small Treg containing compartment among gastric biopsies of GML developing d3Tx mice may play a role in perseverance of a minimal bacterial numbers thereby maintaining an antigen-dependent stimulation and proliferation.
Databáze: OpenAIRE