IFNγ differentially controls the development of idiopathic pneumonia syndrome and GVHD of the gastrointestinal tract
作者： Angela C. Burman , Tatjana Banovic , Rachel D. Kuns , Andrew D. Clouston , Amanda C. Stanley
DOI: 10.1182/BLOOD-2006-12-063982
关键词:
摘要: Although proinflammatory cytokines are key mediators of tissue damage during graft-versus-host disease (GVHD), IFNgamma has previously been attributed with both protective and pathogenic effects. We have resolved this paradox by using wild-type (wt), IFNgamma(-/-), IFNgammaR(-/-) mice as donors or recipients in well-described models allogeneic stem cell transplantation (SCT). show that donor-derived augments acute GVHD via direct effects on (1) the donor T to promote helper 1 (Th1) differentiation (2) gastrointestinal (GI) tract augment inflammatory cytokine generation. However, these detrimental overwhelmed a role preventing development idiopathic pneumonia syndrome (IPS). This is result pulmonary parenchyma prevent migration expansion within lung. Thus, differentially controlling IPS after SCT.
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