T Lymphocyte Plasticity in Autoimmunity and Cancer
1Université Bourgogne Franche-Comté, Dijon, France
2Tbilisi State Medical University, Tbilisi, Georgia
3University Hospital of Dijon, Dijon, France
4University of Arizona, Arizona, USA
T Lymphocyte Plasticity in Autoimmunity and Cancer
Description
T lymphocytes are essential for the development and regulation of adaptive immune responses. Upon engagement of their specific antigen receptor and in presence of appropriate costimulatory signals and specific cytokines, naïve CD4+ and CD8+ T cells differentiate into different effector or suppressor subsets exhibiting distinct phenotypic characteristics and functions. These specialized T lymphocyte subsets may be distinguished by a dedicated transcription factor and cytokine expression profile. Although some of these polarized T-cell subpopulations are typically stable and do not transdifferentiate into other subsets, evidence has been provided that others, such as T helper 1 (Th1), T helper 17 (Th17), or regulatory T (Treg) cells, are characterized by variable degrees of plasticity as demonstrated by their capability to be “reprogrammed” into different suppressor or proinflammatory effector T cells.
We invite investigators to contribute original research articles as well as review articles that seek to address the mechanisms and significance of altered T lymphocyte (CD4+ T helper or CD8+ cytotoxic T lymphocytes) differentiation and function in the pathogenesis of immune-mediated disorders and cancer. A particular interest will be given to papers exploring or discussing the concept of T lymphocyte stability/reprogramming and its relevance in pathological conditions with a specific emphasis on FoxP3+ Treg and Th17 or Th1 cells.
Potential topics include, but are not limited to:
- Altered frequencies and functions of T lymphocyte subsets (Th1, Th2, Th9, Th17, Th22, Tfh, Tr1, and Treg) in the pathogenesis of autoimmune diseases and cancer
- Importance and significance of T lymphocyte plasticity in human diseases
- Molecular and cellular mechanisms responsible for T cell lineage commitment, polarization, and possible reprogramming of T helper (Th1, Th17, Treg, etc.) cells in autoimmunity and cancer
- Treg or Th17 cell stability versus reprogramming in autoimmunity and cancer: controversies and potential therapeutic implications