Donor T-cell production of RANTES significantly contributes to the development of idiopathic pneumonia syndrome after allogeneic stem cell transplantation

Blood. 2005 Mar 15;105(6):2249-57. doi: 10.1182/blood-2004-08-3320. Epub 2004 Nov 16.

Abstract

Idiopathic pneumonia syndrome (IPS) is a major cause of mortality following allogeneic stem cell transplantation (allo-SCT). Clinical and experimental data support a role for conditioning-induced inflammation and alloreactive T-cell responses in IPS pathophysiology, but the mechanisms by which donor leukocytes are ultimately recruited to the lung are not fully understood. RANTES is a chemokine ligand that is up-regulated during inflammation and promotes the recruitment of T cells and macrophages to sites of tissue damage. Using a lethally irradiated murine SCT model (B6 --> B6D2F1), we evaluated the role of donor leukocyte-derived RANTES in the development of IPS. Pulmonary mRNA and protein levels of RANTES were significantly elevated in allo-SCT recipients compared to syngeneic controls and were associated with enhanced mRNA expression of CCR5 and CCR1 and with inflammatory cell infiltration into the lung. Allo-SCT with RANTES-/- donor cells significantly decreased IPS and improved survival. Combinations of allogeneic wild-type or RANTES-/- bone marrow with wild-type or RANTES-/- T cells demonstrated that the expression of RANTES by donor T cells was critical to the development of lung injury after SCT. These data reveal that donor T cells can help regulate leukocyte recruitment to the lung after allo-SCT and provide a possible mechanism through which inflammation engendered by SCT conditioning regimens is linked to allo-specific T-cell responses during the development of IPS.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bone Marrow / immunology
  • Bone Marrow / pathology
  • Bone Marrow Transplantation* / mortality
  • Chemokine CCL5 / deficiency
  • Chemokine CCL5 / immunology*
  • Female
  • Humans
  • Inflammation / etiology
  • Inflammation / immunology
  • Inflammation / pathology
  • Lung / immunology
  • Lung / pathology
  • Lung Injury
  • Macrophages / immunology
  • Macrophages / pathology
  • Mice
  • Mice, Knockout
  • Pneumonia / etiology
  • Pneumonia / immunology*
  • Pneumonia / mortality
  • Pneumonia / pathology
  • Receptors, CCR1
  • Receptors, CCR5 / immunology
  • Receptors, Chemokine / immunology
  • Syndrome
  • T-Lymphocytes / immunology*
  • T-Lymphocytes / pathology
  • Transplantation Conditioning
  • Transplantation, Homologous
  • Up-Regulation / immunology

Substances

  • CCR1 protein, human
  • Ccr1 protein, mouse
  • Chemokine CCL5
  • Receptors, CCR1
  • Receptors, CCR5
  • Receptors, Chemokine