ontact with stroma in an environment of organs. In particular, more should be learned about modulation of stromal cell function by pathogens and inflammatory reactions to consider therapeutic strategies aimed at DC manipulation. So far, shifts in instructive activity of stromal cells regarding immature DCreg development during host-parasite interactions were demonstrated only for leishmania and helminth invasions. We add intracellular mycobacterial pathogens to this list by demonstrating that TB infection differentially affects instructive capacity of lung stroma in genetically TB-susceptible and resistant mice, and that the developing DCreg directly down-regulate the response of mycobacteria-specific CD4+ T lymphocytes. Our 
findings demonstrate that both major cell populations functioning as down-regulators of superfluous T cell immune responses, DCreg and Treg, were more readily developed and more efficiently maintained in mice displaying less severe lung inflammation and pathology in the course of TB infection. These results are in good agreement with those recently published by Leepiyasakulchai et al. who demonstrated similar correlations between the numbers of regulatory dendritic and T cells in the lung, genetic susceptibility to TB challenge and degree of lung pathology. Importantly, their observations concerned a different population of regulatory DC, namely, anti-inflammatory CD103+CD11b-CD11c+ E-DC, whereas in our study we characterized immature CD11b + CD103- DCreg educated on lung stroma. Yet another example 18339876 of pneumonic phagocyte’s involvement 11881984 in immune response inhibition which depends upon mycobacterial infection is an enhanced production of TGF- and PGE2 by pleural macrophages following engulfment of BCG-infected apoptotic neutrophils. Given that the macrophage-rich lung stroma itself is able to directly inhibit T-cell immune responses to several infectious and polyclonal stimuli, we may conclude that a redundancy in the T cell responses suppression system is an essential feature of the lung tissue functioning. This is not surprising, since maintenance of the 5 Regulatory DC in Experimental TB balance between cellular immune responses-mediated MedChemExpress R115777 protection and pathology is critical for successful regulation of overwhelming inflammation affecting mucosal organs during chronic pathologic conditions, such as TB and IBD. Whereas cell populations participating in inhibition of immune responses and inflammation in the lung are impressively diverse, the number of soluble mediators providing suppression which are produced by these cells is small. Production of antiinflammatory cytokine IL-10 is a feature conserved among virtually all systems in which activity of immune response inhibitory cells, such as different regulatory DC and Foxp3+ Treg, has been studied. So far, the reliable list of inhibitory mediators is limited to IL-10, TGF-, NO and PGE2. Our results are in agreement with previous findings: inhibitory activity of supernatants obtained from DCreg educated on lung stroma partly depended upon the presence of PGE2, and the differences in regulatory activity of DCreg obtained from nave and TB-infected mice of susceptible and resistant strains correlated with the differences in IL-10 and NO production. It was not possible to compare the levels of TGF- in supernatants in our system: expansion of DCreg in cocultures with lung stroma is ineffective in the absence of FCS in culture medium, ELISA results are strongly altered due t