The immunomodulatory polysaccharide A, produced by Bacteroides fragilis, induces Foxp3+ IL-10-producing T regulatory cells. Lathrop et al. recently demonstrated that the peripheral T cell population, besides the thymic self/nonself discrimination instructions, further is educated by the colonic microbiota. Recently, the microbiota has also been shown to influence immune responses to LY2157299 TGF-beta inhibitor infections as well as the development of noninfectious conditions. The response towards respiratory tract influenza is altered in antibiotic treated animals suggesting the importance of the microbiota in directing the immune responses at other sites than the gut. In addition, the microbiota also seems to influence development of autoimmune disease and inflammatory bowel disease in mice. Much less is known about how the microbiota influences the human immune system. Although a failure in tolerating the intestinal bacteria is suggested in the pathogenesis of IBD, and an altered early-life colonization pattern associates with the development of allergic diseases, the underlying mechanisms of microbiota-mediated immune modulation in humans need to be further investigated. Early colonization with bifidobacteria has been associated with increased secretory IgA in saliva whereas lactobacilli and bifidobacteria colonization associates with lower cytokine responses and increased Foxp3 expression following in vitro allergen stimulation. Early Bacteroides fragilis colonization seems to associate with immune function also in humans. Infants colonized with Bacteroides fragilis early in life had more IgA-producing cells in infancy, spontaneous IFN-c production and reduced pro-inflammatory responses following LPS stimulation early in life compared to non-colonized infants. In addition, stimulating human immune cells in vitro with bacterial species have demonstrated species-specific immunostimulatory capacities. We have previously reported that infants colonized with lactobacilli rhamnosus, L. paracasei, L. casei) and Bifidobacterium bifidum early in life were significantly less often allergic at five years of age, whereas the opposite tendency was seen for Staphylococcus aureus colonization. Therefore, we wanted to investigate if early-life colonization with these species of bacteria, influences immune responses during childhood. Due to the association between the gut microbiota and T cell development/maturation we choose to stimulate peripheral blood mononuclear cells with the general T cell stimuli phytohaemagglutinin and assessed IFN-c and IL-4 as these cytokines are signature cytokines favoring cell mediated and humoral immunity, respectively, whereas IL-10 was investigated due to its potentially regulatory function. Further, we performed in vitro stimulations of peripheral-blood mononuclear cells with bacterial supernatants to investigate how these species directly induce IL-42, IL-102 and IFN-c production in CD4+ T cells. Studies of germ free and gnotobiotic mice have uncovered the impact of the microbiota on the maturation of both innate and adaptive immune branches of the system. In humans, the role of the microbiota for immune maturation is not as clear. However, there are reports of associations between microbiota composition and immune-mediated disease, although the underlying mechanisms behind these associations are still largely unknown. Based on the hypothesis that the early-life gut microbiota composition influences infant immune maturation, we have investigated early gut bacterial species in relation to numbers of cytokine-secreting cells at two years of age. We clearly demonstrate that infant gut colonization with certain bacterial species associates with the number of cytokine-secreting cells in a speciesspecific manner later in childhood.