Invariant natural killer T (iNKT) cells in HAART-treated, HIV-positive patients with bone and cardiovascular impairment.

In keeping with the evidence of a pro-inflammatory milieu in the pathogenesis of non-infectious diseases in course of HIV [1] , [10] , [11] , subjects with bone impairment showed a trend to higher spontaneous ex vivo TNF secretion and a significant IFN-γ increase release after stimulation, Given the limited number of patients enrolled and the weak statistical significance of such findings we cannot draw definitive conclusions on the role of iNKT cells in bone disease. iNKT cell expression of other members of the TNF superfamily such as RANKL, known to be involved in bone homeostasis, should be explored in such setting.

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In line with the role of IFN-γ–producing iNKT cells in the pathogenesis of atherosclerosis and plaque stability [45] , [51] , we also found a trend to higher IFN-γ secreting iNKT in patients with endothelial damage; this finding did not reach statistical significance, possibly due to limited sample size.

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