It is well established that CD4+ T-helper cells are vital in the adaptive immune response and mediate the clearance of persistent pathogens. Specific T-helper cell phenotypes that secrete distinct profiles of cytokines are generated in response to infection. These cytokines orchestrate homeostasis and pathogen clearance through autocrine and endocrine signalling. Dysregulation of this process can lead to inflammation and autoimmune disease. Secretion of cytokines is facilitated by highly regulated SNARE proteins. SNAREs have been shown to form specific partnerships and facilitate membrane-membrane fusion required for the exocytosis of cytokines and other proteins from immune cells. Using an optimised in vitro model, isolated CD4+ T cells were polarised into T-helper cell subsets in order to profile SNARE expression and regulation. Syntaxin-11 (STX11) was identified as a candidate regulatory SNARE in Th1 and Th17 cells. Further investigation in vivo using two mouse models of inflammation suggested that STX11 was regulated in Th17/Th1 mediated disease. Finally, we examined Th1 and Th17 responses in STX11 deficient mice and demonstrated that in the absence of STX11, T helper cell secreted increased levels of IFN-� and were unable to differentiate into a Th17 subset. The elucidation of SNARE trafficking pathways in CD4+ T-helper cells may represent potential therapeutic targets for blocking cytokine secretion from targeted cells and control inflammation. It may also lead to a better understanding of SNARE deficient immune disorders such as familial haemophagocytic lymphohistocytosis - 4 (FHL-4), characterised by over production of cytokines and high number of activated lymphocytes due to STX11 deficiency.