Prevention of Autoimmunity and Control of Recall Response to Exogenous Antigen by Fas Death Receptor Ligand Expression on T Cells
| Autor: | Salem Chouaib, Christelle Michiels, Imed Mabrouk, Paule Opolon, Stéphanie Buart, Gilles Chiocchia, Saoussen Karray, Meriem Hasmim, Matthieu Lévi-Strauss, Elizabeth Connault |
|---|---|
| Jazyk: | angličtina |
| Předmět: |
Fas Ligand Protein
T-Lymphocytes Immunology chemical and pharmacologic phenomena Biology medicine.disease_cause Fas ligand Autoimmune Diseases Autoimmunity Mice Follicular phase Genotype medicine Animals Immunology and Allergy fas Receptor Antigens MOLIMMUNO Lymphatic Diseases Gene Mice Knockout B-Lymphocytes Recall Germinal center hemic and immune systems Dendritic Cells Infectious Diseases CELLIMMUNO Humoral immunity |
| Zdroj: | Immunity. (6):922-933 |
| ISSN: | 1074-7613 |
| DOI: | 10.1016/j.immuni.2008.10.007 |
| Popis: | Summary Mice with mutations in the gene encoding Fas ligand (FasL) develop lymphoproliferation and systemic autoimmune diseases. However, the cellular subset responsible for the prevention of autoimmunity in FasL-deficient mice remains undetermined. Here, we show that mice with FasL loss on either B or T cells had identical life span as littermates, and both genotypes developed signs of autoimmunity. In addition, we show that T cell-dependent death was vital for the elimination of aberrant T cells and for controlling the numbers of B cells and dendritic cells that dampen autoimmune responses. Furthermore, we show that the loss of FasL on T cells affected the follicular dentritic cell network in the germinal centers, leading to an impaired recall response to exogenous antigen. These results disclose the distinct roles of cellular subsets in FasL-dependent control of autoimmunity and provide further insight into the role of FasL in humoral immunity. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|