| セッション情報 |
Host-microbial Interaction and Immunology in IBD a. Basic Aspects
|
| タイトル |
IF3a-4 Mucosal IgG+CXCR4+ Plasma Cells Contribute to the Pathogenesis of Ulcerative Colitis Through FcγR-mediated Activation of CD14+ Macrophages
|
| 演者 |
|
| 共同演者 |
|
| 抄録 |
Background ＆ Aim ： ln health the maj ority of intestinal plasma cells （PCs） are lgA－producingwhereasthere is a massive influx of lgG－producing PCs into the inflamed血ucosa in ulcerative colitis（UC1）How－everthe precise mechanism of infiltration and their involvement in UC pathogenesis remain unclear．Here we analyzed the characteristics of intestinal PCs in UCand examined the involvement of lgG－immune complex （IC）一FcyR signaling in int．estinal inflammation．Methods ： 1） Microarray gene expression analysis of intestinal PCs was performedand the expression ofcell surface molecules of PCs was analyzed by flow cytometry． 2） Lamina propria mononuclear cells（LPMCs） were stimulated with plate lgG－ICand cytokine production was measured．Results ： 1） The proportion of IgG“ PCs among LP PCs was increased in a correlation with the degree ofmucosal inflammationin UC． Analysis of cell surface molecules revealed that． PCs in infiamed UC mucosawere CD38highCD 19’CD20“CD27iOW unique phenotype． lgG’ PCs in UC highly expressed chemokine recep－tor CXCR4and lacked the expression of CCRIOwhich is expressed in lgA’ PCs． 2） lgG－IC stimulation in－duced the production of inflammatory cytokines sUch as TNF－or from UC LPMCs． We revealed thatCD．14＋intestinal macrophages that are increased in UC mucosa expressed FcyRs and produced TNF－ct byIgG－IC stimulation． FcyR signaling inhibitor selectively inhibited lgG－IC－induced TNF－ct production．Conclusion：Intestinal IgG＋PCs might infiltrate the inflamed mucosa via CXCR4．and be involved in U．C．pathogenesis by exacerbating mucosal inflammation through lgG－IC－FcyR signaling |
| 索引用語 |
|
