It has recently been shown that vitamin D (VitD) plays an important role in host defences, inflammation and immunity. We reviewed PubMed and selected all of the studies published over the last 15 years concerning vun deficiency and VitD supplementation in children with respiratory tract infections.Our analysis showed that VitD seems to be very important because of its part in the complexity of the immune system. However, there are few pediatric studies and most have various limitations. First of all, the literature mainly refers to studies concerning the prevalence of VitD insufficiency and deficiency in specific pathologies. Secondly, it is extremely difficult to identify a common specific range of normal, insufficient and deficient VitD levels. Thirdly, the available studies of VitD supplementation often combined VitD with the use of other micronutrients, thus obscuring the role of VitD itself. Finally, different doses have been used for VitD supplementation. These observations clearly highlight the fact that further studies are needed to evaluate the impact ofVitD deficiency and insufficiency in terms ofthe epidemiology and outcomes of pediatric respiratory tract infection, and whether VitD supplementation favours a positive outcome.Vitamin D (VitD) is a fat-soluble vitamin that has long been known to play a role in calcium homeostasis and bone metabolism (1). The chemical structure ofthe lateral chains ofthe two natural forms of VitD (D2 derived from plants, and D3 derived from humans and animals) are slightly different, and this causes them to bind differently to their carrier proteins. However, the biological activity of their active metabolic products is very similar. Both can be obtained from diet or from sunlight conversion of skin 7-dehydrocholesterol (1). In order to become active, VitD undergoes two different hydroxylations: the first (in position 25) mainly takes place in the liver and involves the mitochondrial 25-hydroxylase enzyme; the second takes place in the proximal kidney tubule and involves the mitochondrial cytochrome P450 enzyme 25-hydroxyvitamin-D-Ia-hydroxylase (1). Most ofthe final product ofVitD is transported in the blood by albumin and vitamin binding proteins, and thus reaches the numerous target tissues with VitD receptors (VitDRs) found throughout the human body. Once it has performed its function, VitD is inactivated by means of 25 (OH)D-24-hydroxylasis into the inactive 24,25-hydroxyvitamin D (1).VitD is essential for the correct development of mineralised bone (1). In the case of a calciumpoor diet, calcitriols interact with the VitDRs on osteoblasts to induce the expression of the RANK cytokine which, by means of various intracellular messages stimulates maturation of osteoclasts and