title: IL-15 stimulates NKG2D while promoting IgM expression of B-1a cells.
abstract: Interleukin (IL)-15, a key manipulator of T-cell function also modulates B-1a cell activity by augmenting activation markers, turning them towards type 1 polarization and immunoglobulin (Ig) expression which is significant in the context of gut immunity. Here we show, for the first time, IL-15 mediated up-regulation of the activation receptor NKG2D and its adaptor DAP10 in B-1a cells indicating their essential coupling with IL-15 receptor signaling pathway. Our results demonstrate IL-15 treatment increases phosphorylation of STAT5 and p38 leading to translocation of NF-κB onto the nucleus, an attribute that delineates activation of B-1a cells and its role in inflammation. In parallel, increase of anti-apoptotic Bcl-xL suggests its role in long term survival of B-1a cells in culture by IL-15. The cytokine induced overexpression of the plasma cell differentiation transcription factor BLIMP-1 while reducing PAX-5a that could be responsible for the spontaneous Ig secretion by B-1a cells. Up-regulation of IgM transcripts in presence of IL-15 validates mucosal response of the cells through natural Abs to counter pathogens.
authors.affiliation: Division of Immunology, National Institute of Cholera and Enteric Diseases, Kolkata, India.
authors.forename: Amlan Kanti
authors.initials: AK
authors.lastname: Ghosh
authors.affiliation: Division of Immunology, National Institute of Cholera and Enteric Diseases, Kolkata, India.
authors.forename: Debolina
authors.initials: D
authors.lastname: Sinha
authors.affiliation: Division of Immunology, National Institute of Cholera and Enteric Diseases, Kolkata, India.
authors.forename: Ratna
authors.initials: R
authors.lastname: Biswas
authors.affiliation: Division of Immunology, National Institute of Cholera and Enteric Diseases, Kolkata, India. Electronic address: shigellaporin@yahoo.com.
authors.forename: Tapas
authors.initials: T
authors.lastname: Biswas
mesh_terms: D000818:Animals; D016175:B-Lymphocyte Subsets / Q000276:immunology* / Q000378:metabolism; D002478:Cells, Cultured; D005260:Female; D005786:Gene Expression Regulation; D007075:Immunoglobulin M / Q000096:biosynthesis* / Q000235:genetics; D019409:Interleukin-15 / Q000502:physiology*; D008297:Male; D008810:Mice, Inbred C57BL; D016328:NF-kappa B / Q000378:metabolism; D055655:NK Cell Lectin-Like Receptor Subfamily K / Q000096:biosynthesis* / Q000235:genetics; D000074462:Positive Regulatory Domain I-Binding Factor 1 / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D011971:Receptors, Immunologic / Q000096:biosynthesis / Q000235:genetics; D050799:STAT5 Transcription Factor / Q000378:metabolism; D015398:Signal Transduction; D015854:Up-Regulation; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: C492355:Hcst protein, mouse; D007075:Immunoglobulin M; D019409:Interleukin-15; C527086:Klrk1 protein, mouse; D016328:NF-kappa B; D055655:NK Cell Lectin-Like Receptor Subfamily K; C513258:Prdm1 protein, mouse; D012333:RNA, Messenger; D011971:Receptors, Immunologic; D050799:STAT5 Transcription Factor; D000074462:Positive Regulatory Domain I-Binding Factor 1; D048051:p38 Mitogen-Activated Protein Kinases
keywords: B-1a cells; IgM; Innate signaling; Interleukin-15