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Blood, 1 August 2007, Vol. 110, No. 3, pp. 1064-1072.
Prepublished online as a Blood First Edition Paper on April 20, 2007; DOI 10.1182/blood-2006-12-063982.
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Submitted December 22, 2006
Accepted April 2, 2007
IFN differentially controls the development of idiopathic pneumonia syndrome and GVHD of the gastrointestinal tract
Angela C Burman, Tatjana D Banovic, Rachel D Kuns, Andrew D Clouston, Amanda C Stanley, Edward S Morris, Vanessa Rowe, Helen Bofinger, Renae Skoczylas, Neil Raffelt, Olivier Fahy, Shaun R McColl, Christian R Engwerda, Kelli P.A. MacDonald, and Geoffrey R. Hill*
Division of Immunology and Infectious Diseases, The Queensland Institute of Medical Research, Brisbane, Australia
Histopath Pathology, Sydney, Australia
Department of Microbiology and Immunology, University of Adelaide, Adelaide, Australia
Department of Bone Marrow Transplantation, Royal Brisbane Hospital, Brisbane, Australia
* Corresponding author; email: geoff.hill{at}qimr.edu.au.
Although proinflammatory cytokines are key mediators of tissue damage during graft-versus-host disease (GVHD), IFN has previously been attributed with both protective and pathogenic effects. We have resolved this paradox by using wild type (wt), IFN-/- and IFNR-/- mice as donors or recipients in well described models of allogeneic stem cell transplantation (SCT). We show that donor-derived IFN augments acute GVHD via direct affects on (i) the donor T cell to promote Th1 differentiation and (ii) the GI tract to augment inflammatory cytokine generation. However, these detrimental effects are overwhelmed by a protective role of IFN 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 IFN is the key cytokine differentially controlling the development of IPS and gastrointestinal GVHD after allogeneic SCT.
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