The first description of involvement of natural CD4+CD25+ Treg cells in regulating immunity to an infectious agent. This paper demonstrates that natural Treg cells can be central to host-pathogen 'détente'. Accumulation of natural Treg cells at sites of chronic infection is responsible for pathogen persistence, a situation that is necessary for the long-term maintenance of memory response.
CD4+CD25+ regulatory T cells control Leishmania major persistence and immunity.
The first report showing that natural Treg cells influence immunity to a virus infection. In this study, the Treg cell effect served to hamper the efficacy of immunity against herpes simplex virus, a situation that became favorable, however, when the immune response resulted in tissue damage.
CD4+CD25+ T cells regulate virus-specific primary and memory CD8+ T cell responses.
The first study that noted that the recall response to an infectious agent was modulated by Treg cells and that their removal resulted in much greater immune responses.
Regulatory CD4+CD25+ T cells restrict memory CD8+ T cell responses.
Kursar, M., Bonhagen, K., Fensterle, J., Kohler, A., Hurwitz, R., Kamradt, T., Kaufmann, S.H. & Mittrucker, H.W.
Two reports showing the notable discovery that viral infection induces Treg cells. Chronic viral infection in humans was correlated with the induction of virus-specific Treg cells.
Immunosuppression by CD4+ regulatory T cells induced by chronic retroviral infection.
Iwashiro, M., Messer, R.J., Peterson, K.E., Stromnes, I.M., Sugie, T., & Hasenkrug, K. J.
First report demonstrating that CD4+ Treg cells induced by chronic exposure to infectious agents can, via interleukin 10-producing dendritic cells, suppress antigen-specific responses to pathogen.
Pathogen-specific T regulatory 1 cells induced in the respiratory tract by a bacterial molecule that stimulates interleukin 10 production by dendritic cells: a novel strategy for evasion of protective T helper type 1 responses by Bordetella pertussis.
The first report that emphasized that a chief function of natural Treg cells is to diminish tissue-damaging inflammatory reactions to an infection agent.
CD25+CD4+ regulatory T cells suppress CD4+ T cell-mediated pulmonary hyperinflammation driven by Pneumocystis carinii in immunodeficient mice.
This report demonstrates involvement of natural Treg cells in the prevention of intestinal inflammation caused by infectious agents. The effect seemed to be directed to innate inflammatory reactions through mechanisms mediated by interleukin 10 or transforming growth factor-Β.
