Finally, the IL-10 (Th2) reduction could be suggestive of its therapeutic use in TAO. Based on the unclear TAO pathogenesis, particularly the involvement of immune trigger mechanisms of vascular disease, further studies should be carried out to reveal the role of the immune disorder in TAO progression. Finally, the discovery of IL-17 and its association with inflammation and autoimmune pathology

has reshaped our viewpoint regarding the pathogenesis of TAO, which was based previously on the Th1–Th2 paradigm. The inflammatory profile status is not exclusive to TAO; in other diseases, where damage to the vascular wall is recorded, the scenario of increased proinflammatory and detrimental anti-inflammatory Selleckchem LBH589 cytokines has also been described buy Seliciclib for other types of vasculitis. In order to analyse the behaviour/onset of inflammatory status, it would be useful to have evidence of those cytokine profiles in healthy smokers along the time course of consumption and in non-diseased TAO patients. Unfortunately, we could not obtain this information from consulting the patients’ charts. In addition

to the Th17 profile, the development of autoimmunity could be defined clearly by monitoring autoantibodies and autoreactive T cells along the time course of TAO, which was not performed in the present study. None. This work was supported in part by FAEPA (HCFMRP/USP), CNPq and FAPESP 09/50508-5. “
“Precise identification of NK-cell populations in humans and nonhuman primates has been confounded by imprecise phenotypic definitions. A common definition used in nonhuman primates, including chimpanzees, is CD3−CD8α+CD16+, and this is the dominant NK-cell phenotype in peripheral

blood. However, recent data suggest that in chimpanzees a rare CD8α−CD16+ population also exists. Herein, we present evidence validating the existence of this rare subset in chimpanzee peripheral blood, but also demonstrating that gating on CD3−CD8α−CD16+ cells can inadvertently include a large number of CD16+ myeloid DCs (mDCs). We confirmed the inclusion of mDCs in CD3−CD8α−CD16+ gated cells by demonstrating high expression of CD11c, BDCA-1 and HLA-DR, and by Cyclin-dependent kinase 3 the lack of expression of NKp46 and intracellular perforin. We also functionally validated the CD8α− NK-cell and mDC populations by mutually exclusive responsiveness to a classical NK-cell stimulus, MHC class I-deficient cells, and a prototypic mDC stimulus, poly I:C, respectively. Overall, these data demonstrate common problems with gating of NK cells that can lead to erroneous conclusions and highlight a critical need for consensus protocols for NK-cell phenotyping. Because of their potent ability to kill virus-infected or neoplastic cells without prior sensitization, NK cells are often characterized as the major effector cells of the innate immune system.