Finally, the role of the inflammasome in host defense (e.g. influenza) and disease pathogenesis (e.g. cerebral malaria, Alzheimer’s disease, diabetes) remains poorly understood. Work in our laboratory is supported by NIH grants AI063331, AI064748 and AI064748. We thank Jurg Tschopp for sharing manuscript prior to publication. L. F. was a recipient of a postdoctoral fellowship from the Arthritis Foundation. Cisplatin ic50 T. E. was supported by a Fellowship from the Deutsche Forschungsgemeinschaft (DFG) Germany and T.
R. by a Fellowship from the Swiss National Science Foundation. We apologize to many investigators whose important work was not explicitly cited due to space constrains. Conflict of interest: The authors declare no financial or commercial conflict of interest. See accompanying Viewpoint: http://dx.doi.org/10.1002/eji.200940207 “
“The pathogenesis of nasal polyposis remains unclear; it severely affects patients’ quality of life and complicates inflammation in adjacent organs such as sinusitis and asthma. Aberrant immune regulatory function in these patients is proposed. The present study aims to examine the regulatory T cells (Treg) in nasal mucosa of patients with allergic rhinitis (AR) and nasal polyposis (NP). Patients with AR or AR/NP were
treated with inferior turbinectomy for their inferior turbinate hyperplasia. Surgically removed nasal mucosa was collected to examine the Treg by immunohistochemistry and flow cytometry. The results showed that more forkhead box P3 (FoxP3)+ cells were found in AR with polyps than in those with AR alone. Further studies revealed that these FoxP3+ learn more T cells from AR/NP group also expressed interleukin (IL)-17. In vitro study showed that staphylococcal enterotoxin B (SEB) induced CD4+ FoxP3+ T cells to become FoxP3+ IL-17+ cells via facilitating the expression of IL-6, that in synergy with transforming growth factor-beta, induce the expression of IL-17 in FoxP3+ cells. We conclude that FoxP3+ IL-17+ T cells were localized in the nasal mucosa of Celecoxib patients with AR and NP. SEB may play a role in converting FoxP3+ Treg to FoxP3+ IL-17+ T cells. The presence of IL-17+ FoxP3+ T cells
may play a role in the remodelling of the nasal airways in certain people who develop polyps, irrespective of whether or not they are atopic. It has been noted that a correlation exists between nasal allergy (AR) and nasal polyposis (NP) [1–3]; however, the underlying mechanism remains to be further understood. Functional deficiency or decrease in the number of regulatory T cells (Treg) plays a critical role in allergic diseases [4]. However, the properties of Treg in upper airway mucosa need to be further elucidated. Forkhead box P3 (FoxP3) is a transcription factor in CD4+ CD25+ Treg that is regarded as a signature molecule in CD4+ Treg[5]. Recent studies indicate that there is a subset of CD4+ FoxP3+ T cells that express interleukin (IL)-17 [6,7].