9 It has been suggested that targeting IL-13

alone or in combination with IL-4 may be more Angiogenesis inhibitor useful in combating asthma.139 Also, a mutated IL-4 that targets IL-4Rα, thereby blocking the effects of IL-4 and IL-13, is also being developed.140 Other strategies that target IL-5 and tumour necrosis factor-α have been proposed, but the benefits of using biological modifiers need to be weighed against the risks of unwanted effects before they can be put into clinical use. The type-2 microenvironment has been re-structured over the past 5 years with the born-again basophil providing early IL-4 and with the capacity to process and present antigen to Th cells. At 90 degrees to this interaction is the discovery of innate-like cells with the

capacity to secrete large amounts of IL-5, IL-13 and IL-9, triggering type-2 responses, presumably before the clonal expansion of antigen-restricted Th2 cells. Finally, the observation that Th2 cells can develop into Th1,5 Th176 or ‘Th9’3 cells with the appropriate environmental cues suggest a great degree of plasticity within the Th cell populations. However, while these newer discoveries fill in the gaps of the type 2 environment and have tended to down-grade the Th2 cell into a co-star role, there is still a great deal we do not know about Th2 cells. If antigen this website specificity and memory Th responses are required for improved vaccine efficacy, either directly or via antibody production, and if allergen-reactive T cells are responsible for atopic disorders, then investigating how these newer discoveries impact Th2 cell development and their effector function in this context remains an important area of

research. We gratefully thank the MRC and Lady TATA foundation for supporting MSW and ISO. We also thank Nicholas Mathioudakis and Stephanie Czieso for helpful discussions. “
“A dilemma in cancer immunology is that, although patients often develop active antitumor immune responses, the tumor still outgrows. It has become clear that under the pressure of the host’s immune system, PIK3C2G cancer cells have adapted elaborate tactics to reduce their immunogenicity (also known as immunoselection) and/or to actively suppress immune cells and promote immune tolerance (also known as immunosubversion). In this issue of the European Journal of Immunology, Dolen and Esendagli [Eur. J. Immunol. 2013. 43: 747–757] show that acute myeloid leukemia (AML) cells develop an adaptive immune phenotype switching mechanism: In response to attack by activated T cells, the leukemia cells quickly downregulate the T-cell costimulatory ligand B7-H2 and reciprocally upregulate the coinhibitory ligands B7-H1 and B7-DC in order to shut down T-cell activation via the PD-1 pathway.