免疫学
促炎细胞因子
移植物抗宿主病
胃肠道
细胞因子
肺炎
医学
移植
肺
干细胞
免疫系统
生物
炎症
内科学
遗传学
作者
Angela C. Burman,Tatjana Banovic,Rachel D. Kuns,Andrew D. Clouston,Amanda C. Stanley,Edward S. Morris,Vanessa Rowe,Helen M. Bofinger,Renae Skoczylas,Neil C. Raffelt,Olivier Fahy,Shaun R. McColl,Christian Engwerda,Kelli P. A. McDonald,Geoffrey R. Hill
出处
期刊:Blood
[American Society of Hematology]
日期:2007-08-01
卷期号:110 (3): 1064-1072
被引量:163
标识
DOI:10.1182/blood-2006-12-063982
摘要
Abstract Although proinflammatory cytokines are key mediators of tissue damage during graft-versus-host disease (GVHD), IFNγ has previously been attributed with both protective and pathogenic effects. We have resolved this paradox by using wild-type (wt), IFNγ−/−, and IFNγR−/− mice as donors or recipients in well-described models of allogeneic stem cell transplantation (SCT). We show that donor-derived IFNγ augments acute GVHD via direct effects on (1) the donor T cell to promote T helper 1 (Th1) differentiation and (2) the gastrointestinal (GI) tract to augment inflammatory cytokine generation. However, these detrimental effects are overwhelmed by a protective role of IFNγ in preventing the development of idiopathic pneumonia syndrome (IPS). This is the result of direct effects on pulmonary parenchyma to prevent donor cell migration and expansion within the lung. Thus, IFNγ is the key cytokine differentially controlling the development of IPS and gastrointestinal GVHD after allogeneic SCT.
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