caa a22 4500 467907773 CHVBK 20180406152839.0 cr unu---uuuuu 170328e20060101xx s 000 0 eng 10.1007/s00251-005-0057-2 doi (NATIONALLICENCE)springer-10.1007/s00251-005-0057-2 LST1 and NCR3 expression in autoimmune inflammation and in response to IFN-γ, LPS and microbial infection [Elektronische Daten] [H. Mulcahy, K. O'Rourke, C. Adams, M. Molloy, F. O'Gara] Many genes in the central region of the major histocompatibility complex (MHC) encode proteins involved in immune and inflammatory responses. In this study, we have further characterized two genes in the MHC class IV region, leucocyte-specific transcript (LST) 1 and natural cytotoxicity-triggering receptor 3 (NCR3) (also known as 1C7 and natural killer (NK)p30). The specific function of LST1 is not known, although expression analysis and functional data suggest an immunomodulatory role. The LST1 gene undergoes extensive alternative splicing, giving rise to both membrane-bound (encoded by exon 3) and soluble isoforms. The NCR3 protein is involved in NK-mediated cytotoxicity and plays a role in NK/dendritic cell crosstalk. Expression of these genes was examined, by real-time reverse transcriptase-polymerase chain reaction, in autoimmune-induced inflammation, specifically rheumatoid-arthritis-affected blood and synovium, and in response to stimulation with inflammatory mediators and bacterial agents. The expression of LST1, specifically splice variants encoding soluble isoforms and NCR3, was increased in rheumatoid-arthritis-affected blood and synovium and was associated with more severe inflammation in the synovium. Furthermore, both genes were significantly up-regulated in response to lipopolysaccharide, interferon (IFN)-γ and bacterial infection. These findings suggest that NCR3 and soluble isoforms of LST1 may play a role in inflammatory and infectious diseases. Springer-Verlag, 2005 LST1 nationallicence NCR3 nationallicence Immunity nationallicence Rheumatoid arthritis nationallicence Mulcahy H. BIOMERIT Research Centre, Department of Microbiology, University College Cork, Cork, Ireland aut O'Rourke K. BIOMERIT Research Centre, Department of Microbiology, University College Cork, Cork, Ireland aut Adams C. BIOMERIT Research Centre, Department of Microbiology, University College Cork, Cork, Ireland aut Molloy M. Department of Rheumatology, Cork University Hospital, Cork, Ireland aut O'Gara F. BIOMERIT Research Centre, Department of Microbiology, University College Cork, Cork, Ireland aut Immunogenetics Springer-Verlag 57/12(2006-01-01), 893-903 0093-7711 57:12<893 2006 57 251 https://doi.org/10.1007/s00251-005-0057-2 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s00251-005-0057-2 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Mulcahy H. BIOMERIT Research Centre, Department of Microbiology, University College Cork, Cork, Ireland aut NATIONALLICENCE 700 1- O'Rourke K. BIOMERIT Research Centre, Department of Microbiology, University College Cork, Cork, Ireland aut NATIONALLICENCE 700 1- Adams C. BIOMERIT Research Centre, Department of Microbiology, University College Cork, Cork, Ireland aut NATIONALLICENCE 700 1- Molloy M. Department of Rheumatology, Cork University Hospital, Cork, Ireland aut NATIONALLICENCE 700 1- O'Gara F. BIOMERIT Research Centre, Department of Microbiology, University College Cork, Cork, Ireland aut NATIONALLICENCE 773 0- Immunogenetics Springer-Verlag 57/12(2006-01-01), 893-903 0093-7711 57:12<893 2006 57 251 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer