Editorial CD4 + T Helper Cell Plasticity in Infection, Inflammation, and Autoimmunity Samuel Huber, 1 Nicola Gagliani, 1,2 William O’Connor Jr., 3 Jens Geginat, 4 and Flavio Caprioli 5 1 Department of Medicine, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany 2 Department of General, Visceral and Toracic Surgery, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany 3 Department of Immunology and Microbial Disease, Albany Medical Center, Albany, NY, USA 4 Istituto Nazionale di Genetica Molecolare Romeo ed Enrica Invernizzi, Milan, Italy 5 Gastroenterology and Endoscopy Unit, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Milan, Italy Correspondence should be addressed to Samuel Huber; shuber@uke.de Received 2 January 2017; Accepted 4 January 2017; Published 29 January 2017 Copyright © 2017 Samuel Huber et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. CD4 T helper (T H ) cells orchestrate the immune response and play a pivotal role in infection, infammation, and autoimmunity. CD4 T H cells can be subdivided into diferent subsets, which are defned based on a specifc network of transcriptional regulators and unique cytokine profles. Tis model despite its limitation has proven to be useful to understand the complexity of the immune system and its rela- tionship to diferent types of immune mediated infammatory diseases. Interestingly recent fndings indicate that some T H cell subsets have a certain degree of plasticity. Tey can share characteristics typical of other types of T H cells and poten- tially lose their original features to convert into another T H cell subset. Tis has been shown for all known T H cell subset but best studied for T H 17 cells [1, 2]. Tus T H 17 cells have the capacity to acquire a T H 1 phenotype under chronic infamma- tion [3, 4] but can also convert to regulatory T cells [5–9] and participate in the resolution of the immune response [5, 7–9]. Tese basic aspects of T H cell lineages and plasticity are discussed by J. E. Beliz´ ario et al. who focused on thymic and postthymic regulation of na¨ ıve CD4 + T cell lineage fates in humans and mouse models. Furthermore M. L. Diller et al. described the link between T H 17 and regulatory T cells highlighting the mechanisms driving T H 17 cells plasticity and discussed the biologic consequences of their unique relationship. T helper cell plasticity seems to play a key role in ampli- tude of diseases. Accordingly L. Barbarash et al. analyzed T cell response in patients with implanted biological and mechanical prosthetic heart valves. Teir fndings suggest that altered composition of T cell subsets correlates with the development of xenograf rejection. Furthermore A. Ni et al. studied T H 17 cell response following motor nerve injury in mice. Tey found that motor nerve injury exacerbates T H 17 cell responses, which may contribute to the development of amyotrophic lateral sclerosis. J. Ruhnau et al. reported reduced numbers and impaired function of regulatory T cells in peripheral blood of ischemic stroke patients. C. F. Krebs and O. M. Steinmetz review the role of CD4 + T cell fate in glomerulonephritis. Interestingly, T H 17 cells seem to have a relatively stable phenotype and regulatory T cells show het- erogeneity rather than plasticity during glomerulonephritis. Tese fndings suggest that the environment plays a key role during T helper cell plasticity. In conclusion, we hypothesize that the study of T H cell plasticity could pave the way for future therapies aiming to steer an immune response towards the desired outcome. However, it is unclear at which stage of maturation T H cells will lose their potential plasticity and if T cell plasticity plays an essential role during physiological immune responses or whether it is merely a tolerable “mistake” which does not provide any physiological advantage. If this latter point would turn out to be true, this will not exclude the possibility of reprogramming the immune system but this reprogramming will probably lead to more side efects. Hindawi Mediators of Inflammation Volume 2017, Article ID 7083153, 2 pages https://doi.org/10.1155/2017/7083153