Rajashree P, Supriya

P, Das SD: Differential migration of human monocyte-derived dendritic cells after infection with prevalent clinical strains of Mycobacterium tuberculosis . Immunobiology 2008,213(7):567–575.PubMedCrossRef 65. Bansal K, Sinha AY, Ghorpade DS, Togarsimalemath SK, Patil SA, Kaveri SV, Balaji KN, Bayry J: Src homology 3-interacting domain of Rv1917c of Mycobacterium tuberculosis induces selective maturation of human dendritic cells by regulating PI3K-MAPK-NF-κB signaling and drives Th2 immune responses. Journal of Biological Angiogenesis inhibitor Chemistry 2010,285(47):36511–36522.PubMedCrossRef 66. Wang C, Peyron P, Mestre O, Kaplan G, van Soolingen D, Gao Q, Gicquel B, Neyrolles O: Innate immune response to Mycobacterium tuberculosis Beijing and other genotypes. PLoS ONE 2010,5(10):e13594.PubMedCrossRef 67. Torchinsky MB, Garaude J, Martin AP,

Blander JM: Innate immune recognition of infected apoptotic cells directs Lenvatinib supplier T H 17 cell differentiation. Nature 2009,458(7234):78–82.PubMedCrossRef 68. Nakano H, Nagata T, Suda T, Tanaka T, Aoshi T, Uchijima M, Kuwayama S, Kanamaru N, Chida K, Nakamura H, Okada M, Koide Y: Immunization with dendritic cells retrovirally transduced with mycobacterial antigen 85A gene elicits the specific cellular immunity Selleck Q-VD-Oph including cytotoxic T-lymphocyte activity specific to an epitope on antigen 85A. Vaccine 2006,24(12):2110–2119.PubMedCrossRef 69. Keane J, Shurtleff B, Kornfeld H: TNF-dependent BALB/c murine macrophage apoptosis following Mycobacterium tuberculosis infection inhibits bacillary growth in an IFN-γ independent manner. Tuberculosis 2002,82(2–3):55–61.PubMedCrossRef Authors’ contributions RCMR performed the experiments and prepared

the figures; MPOS performed the cytokine ELISAs; RCMR and MPOS analysed the data; MPOS and JK conceived of and designed the study; RCMR, MPOS Adenosine triphosphate and JK wrote the manuscript. All authors read and approved the final manuscript.”
“Background Acquisition of genomic islands (GIs) plays a key role in bacterial evolution [1, 2]. In silico analyses revealed that numerous GIs probably belong to Integrative and Conjugative Elements (ICEs) or are ICE-deriving elements [3, 4]. ICEs, including conjugative transposons, were defined as autonomous mobile elements that encode the functions needed for their excision, conjugative transfer and integration [3]. Cis-acting sequences and genes involved in a same biological process (for example conjugation) are generally grouped in a module, such as oriT and genes encoding relaxosome and conjugation pore. The recombination, conjugation and regulation modules are frequently grouped to form the core region of the ICEs. Although ICEs replicate during their conjugative transfer, it was originally assumed that they are incapable of autonomous intracellular replication and that their maintenance during cell growth and division only relies on their integration in the chromosome.