Abstract
Control of IFN-γ-secreting T helper (Th) 1 cells prevents autoimmunity and immunopathology during infection. IL-10-mediated suppression of Th1 cells is achieved not only through IL-10 produced extrinsically, but also through a negative feedback loop that induces " intrinsic" IL-10 expression in cells also expressing IFN-γ, during Th1 lineage differentiation. Targeting this Th1 cell IFN-γ to IL-10 switching is a tantalising prospect for developing therapeutics for Th1-mediated diseases. In this review, the molecular pathways that regulate IFN-γ versus IL-10 expression in Th1 cells are examined, with focus on the role of complement regulator and T cell co-stimulatory molecule CD46, and also discussed are challenges and controversies in the field.
| Original language | English |
|---|---|
| Journal | Trends in Immunology |
| Volume | 32 |
| Issue number | 6 |
| Pages (from-to) | 278-286 |
| Number of pages | 9 |
| ISSN | 1471-4906 |
| DOIs | |
| Publication status | Published - 06.2011 |
Funding
Research in the Cope and Kemper laboratories is supported by Arthritis Research UK, The Wellcome Trust, the Medical Research Council (MRC) and The Nuffield Foundation, the EU-funded Innovative Medicines Initiative BTCURE, the MRC Centre for Transplantation, Guy's Hospital, King's College, and the Department of Health, National Institute for Health Research (NIHR) comprehensive Biomedical Research Centre award to Guy's & St Thomas’ NHS Foundation Trust, in partnership with King's College London and King's College Hospital NHS Foundation Trust.
Research Areas and Centers
- Academic Focus: Center for Infection and Inflammation Research (ZIEL)
