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Antibiotic susceptibility of S. aureuswas retrospectively assessed in 1833 strains isolated from skin lesions observed in an Italian tertiary care hospital. Methicillin resistance was more frequent in outpatients than in inpatients (18% vs. 14%, p = 0.04) as well as resistance to cotrimoxazole (8% vs. 4.1%, p < 0.001). Resistance to ampicillin was 99% in both groups, while for clindamycin it was 11% and 14%, respectively. Among topical antibiotics fusidic acid showed the better resistance profile (3%). Antibiotic resistance in pediatric skin infection in outpatients could represent a therapeutic problem in Italy.

Natural killer (NK) cells are lymphoid effectors that are involved in the innate immune  surveillance against infected and/or tumor cells. Their function is under the fine-tuning  control of cell surface receptors that display either inhibitory or activating function and in  healthy condition, mediate self-tolerance. It is known that inhibitory receptors are  characterized by clonal and stochastic distribution and are extremely sensible to any  modification, down-regulation or loss of MHC class I surface expression that  are  induced in autologous cells upon viral infection or cancer transformation. This alteration  of the MHC class I expression weakens the strength of the inhibitory receptor-induced  interaction, thus resulting in a prompt triggering of NK cell function, which ends up in  the inhibition of tumor progression and proliferation of pathogen-infected cells. Thus, the  inhibitory function of NK cells is only one face of the medal, since NK cell activation is  controlled by different arrays of activating receptors that finally are involved in the  induction of NK-mediated cytolysis and/or cytokine releases. Interestingly, the inhibitory  NK cell receptors that are involved in dampening NK cell-mediated responses evolved  during speciation in different, often structurally unrelated surface-expressed molecules,  but all using a conserved signaling pathway. In detail, during evolution, the inhibitory  receptors that assure the recognition of MHC class I molecules, originate in, at least,  three different ways. This ended up in multigene families showing marked structural  divergences that coevolved in a convergent way with the availability of appropriate MHC  ligand molecules.

MHC-specific Natural Killer inhibitory receptors display a conserved and fundamental function in the regulation of NK-mediated cytolysis. Their importance is substantiated by the fact that during speciation different molecular receptor structures have evolved to maintain inhibitory regulation of NK cells. The information gained during these last twenty years begins to be fruitfully used in the therapy of leukemias, but a lot has to be still done. In particular, we need to understand the role of activating KIR and their ligand(s), since their role in the course of different viral diseases is still intriguing.

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