التفاصيل البيبلوغرافية
| العنوان: |
CD28 Deficiency Enhances Type IIFN Production by Murine Plasmacytoid Dendritic Cells. |
| المؤلفون: |
Macal, Monica1, Tam, Miguel A.1, Hesser, Charles1, Di Domizio, Jeremy2, Leger, Psylvia1, Gilliet, Michel2, Zuniga, Elina I.1 eizuniga@ucsd.edu |
| المصدر: |
Journal of Immunology. 2/15/2016, Vol. 196 Issue 4, p1900-1909. 10p. |
| مصطلحات موضوعية: |
*DENDRITIC cells, *AUTOIMMUNE diseases, *GENE expression, *T cells, *VIRUS diseases, *ANTIVIRAL agents, *ANTI-infective agents |
| مستخلص: |
Type I IFNs (IFN-I) are key innate mediators that create a profound antiviral state and orchestrate the activation of almost all immune cells. Plasmacytoid dendritic cells (pDCs) are the most powerful IFN-I-producing cells and play important roles during viral infections, cancer, and autoimmune diseases. By comparing gene expression profiles of murine pDCs and conventional DCs, we found that CD28, a prototypic T cell stimulatory receptor, was highly expressed in pDCs. Strikingly, CD28 acted as a negative regulator of pDC IP'N-I production upon TLR stimulation but did not affect pDC survival or maturation. Importantly, cellintrinsic CD28 expression restrained pDC (and systemic) IFN-I production during in vivo RNA and DNA viral infections, limiting antiviral responses and enhancing viral growth early after exposure. Finally, CD28 also downregulated IFN-I response upon skin injury. Our study identified a new pDC regulatory mechanism by which the same CD28 molecule that promotes stimulation in most cells that express it is co-opted to negatively regulate pDC IFN-I production and limit innate responses. [ABSTRACT FROM AUTHOR] |
| قاعدة البيانات: |
Academic Search Index |
