Fas/FasL Signaling Regulates CD8 Expression During Exposure to Self-Antigens

Frontiers in Immunology

卷:12

Rosa M. Rubio¹  Noé Rodríguez-Rodríguez¹  Florencia Rosetti¹  Iris K. Madera-Salcedo¹  José C. Crispín²  Giovanna Flores-Mendoza³ 

[1] Departamento de Inmunología y Reumatología, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico;

[2] Escuela de Medicina y Ciencias de la Salud, Tecnologico de Monterrey, Monterrey, Mexico;

[3] Posgrado en Ciencias Biológicas, Universidad Nacional Autónoma de México (UNAM), Mexico City, Mexico;

关键词: CD8;    CD95;    Fas;    FasL;    tolerance;    double negative T cell;   

DOI  :  10.3389/fimmu.2021.635862

来源: DOAJ

【 摘 要 】

Activation of self-reactive CD8+ T cells induces a peripheral tolerance mechanism that involves loss of CD8 expression. Because genetic deficiency of Fas and Fasl causes the accumulation of double-negative (DN; CD3+ TCR-αβ+ CD4- CD8-) T cells that have been proposed to derive from CD8+ cells, we decided to explore the role of Fas and FasL in self-antigen-induced CD8 downregulation. To this end, we quantified Fas and FasL induction by different stimuli and analyzed the effects of Fas/FasL deficiency during a protective immune response and after exposure to self-antigens. Our data describes how Fas and FasL upregulation differs depending on the setting of CD8 T cell activation and demonstrates that Fas/FasL signaling maintains CD8 expression during repetitive antigen stimulation and following self-antigen encounter. Together, our results reveal an unexpected role of Fas/FasL signaling and offer a new insight into the role of these molecules in the regulation of immune tolerance.

【 授权许可】

Unknown