CD4+CD25+ suppressor T cells regulate pathogen induced inflammation and disease.
A key suppressor role has recently been ascribed to the natural CD4+CD25+ regulatory T cells (Treg), the removal of which leads to the development of autoimmune disease and aggravated pathogen-induced inflammation in otherwise normal hosts. The repertoire of antigen specificities of Treg is as broad as that of naive T cells, recognizing both self and non-self antigens, enabling Treg to control a broad range of immune responses. Although widely acknowledged to play a role in the maintenance of self-tolerance, recent studies indicate that Treg can be activated and expanded against bacterial, viral and parasite antigens in vivo. Such pathogen-specific Treg can prevent infection-induced immunopathology but may also increase the load of infection and prolong pathogen persistence by suppressing protective immune responses. This review discusses the role of Treg in the prevention of exaggerated inflammation favoring chronicity in bacterial or fungal infections and latency in viral infections. Special attention is given to the role of Treg in the modulation of gastric inflammation induced by Helicobacter pylori infection. Findings in both experimentally infected mice and humans with natural infection indicate that Treg are important in protecting the H. pylori-infected host against excessive gastric inflammation and disease symptoms but on the negative side promote bacterial colonization at the gastric and duodenal mucosa which may increase the risk in H. pylori-infected individuals to develop duodenal ulcers.
Raghavan
Sukanya
S
Department of Medical Microbiology and Immunology, The Göteborg University Vaccine Research Institute (GUVAX), P.O. Box 435, 405 30 Göteborg, Sweden. sukanya.raghavan@microbio.gu.se
Holmgren
Jan
J
D000818:Animals; D015704:CD4 Antigens / Q000378:metabolism*; D005756:Gastritis / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D016481:Helicobacter Infections / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D016480:Helicobacter pylori / Q000276:immunology / Q000472:pathogenicity; D006801:Humans; D007239:Infections / Q000209:etiology / Q000276:immunology*; D007249:Inflammation / Q000209:etiology / Q000276:immunology*; D051379:Mice; D015375:Receptors, Interleukin-2 / Q000378:metabolism*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*
D015704:CD4 Antigens; D015375:Receptors, Interleukin-2