Autoimmunity co-signaling system: Regulatory T cells, CTLA-4 and FOXP3
Co-signaling molecules can act as co-stimulators or co-inhibitors, depending on whether they promote or suppress T-cell activation, respectively. At the specific time and location, co-signaling molecules positively and negatively control antigen presentation, growth, differentiation and function of...
| Autores: | , , |
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| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2005 |
| País: | Colombia |
| Institución: | Universidad del Rosario |
| Repositorio: | Repositorio EdocUR - U. Rosario |
| Idioma: | inglés |
| OAI Identifier: | oai:repository.urosario.edu.co:10336/24315 |
| Acceso en línea: | https://repository.urosario.edu.co/handle/10336/24315 |
| Access Level: | acceso abierto |
| Palabra clave: | Cytotoxic T lymphocyte antigen 4 Transcription factor FOXP3 Antigen presentation Autoimmunity Cell differentiation Cell function Cell stimulation Gene repression Genetic transcription Human Molecular dynamics Nonhuman Promoter region Review Signal transduction T lymphocyte Autoimmune Diabetes Co-signaling CTLA-4 FOXP3 Regulatory T cells Rheumatoid Arthritis Systemic Lupus Erythematosus |
| Sumario: | Co-signaling molecules can act as co-stimulators or co-inhibitors, depending on whether they promote or suppress T-cell activation, respectively. At the specific time and location, co-signaling molecules positively and negatively control antigen presentation, growth, differentiation and function of T-cells. An important cellular group implicated in the regulation of co-stimulation is known as regulatory T cells (Treg). These cells can be used clinically in treatments ranging from cellular transfer in transplant patients to autoimmune diseases and suppression in cancer patients. Treg act through CTLA-4 molecules, which have the ability to suppress the co-stimulation signals and to stop the T cell response. Recently, CTLA-4Ig fusion molecules have been developed, which can block the presentation of auto-antigens. FOXP3 transcription factor is a specific molecule present in Treg that inhibits the production of IL-2 by CD4+ activated cells. Currently, FOXP3 functions are being extensively studied in order to develop new therapeutic targets. This article reviews co-signaling and its mechanism in Treg (CTLA-4, FOXP3), as well as its role in the physiopathology of autoimmune diseases. |
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