CD4+T Helper Cell Plasticity in Infection, Inflammation, and Autoimmunity
1University Medical Center Hamburg-Eppendorf Martinistr, Hamburg, Germany
2Yale University, New Haven, USA
3Albany Medical Center, Albany, USA
4Istituto Nazionale di Genetica Molecolare (INGM), Milan, Italy
5Universita degli Studi di Milano (UNIMI), Milan, Italy
CD4+T Helper Cell Plasticity in Infection, Inflammation, and Autoimmunity
Description
CD4+ T helper cells have been classically divided into different lineages. However recent data have challenged this paradigm: both T helper cell instability (they can cease to express their respective signature cytokine) and plasticity (they can start expressing cytokines typical of other lineages) have been observed. Furthermore this process seems to play a major role during infection, chronic inflammation, and carcinogenesis. However the factors controlling this phenomenon have only recently been uncovered.
We invite authors to contribute original research articles as well as review articles that will illustrate and stimulate the continued effort to understanding the mechanisms regulating T helper cell plasticity and instability and the consequences in different diseases.
Potential topics include, but are not limited to:
- Recent discoveries of T helper cell plastic and instability in infection, autoimmunity, chronic inflammation, and carcinogenesis
- Mechanism regulating T helper cell plasticity and instability
- Consequences of T helper cell plasticity and instability in diseases.
- Potential way to therapeutically manipulate T helper cell plasticity instability
- T helper cell plasticity and instability in human diseases and in T cell therapies