期刊
BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
卷 7, 期 7, 页码 368-377出版社
ELSEVIER SCIENCE INC
DOI: 10.1053/bbmt.2001.v7.pm11529486
关键词
ICAM-1; allogeneic BMT; idiopathic pneumonia syndrome
资金
- NHLBI NIH HHS [R01 HL55952] Funding Source: Medline
- NIAID NIH HHS [R01 AI 34495, P01 AI 35225] Funding Source: Medline
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [P01AI035225, R01AI034495] Funding Source: NIH RePORTER
Following allogeneic bone marrow transplantation (alloBMT), idiopathic pneumonia syndrome (TPS) and graft-versus-host disease (GVHD) caused by donor cell alloreactivity remain major obstacles to a successful outcome. Intercellular adhesion molecule-1 (ICAM-1) is an adhesion molecule that is involved in regulating lymphohematopoietic cell migration and facilitating T-cell responses. To determine whether ICAM-1 expression in the host would affect IPS or GVHD tissue injury responses, ICAM-1(-/-) mice were compared with ICAM-1(+/+) controls. ICAM-1(-/-) recipients did not exhibit the manifestations of IPS injury such as an increase in lung weights nor decreased lung function. The influx of T cells, macrophages, and neutrophils was dramatically dampened as was the production of the inflammatory cytokines interferon-gamma and tumor necrosis factor a and the chemokines monocyte chemotactic protein 1, macrophage inflammatory protein 1 alpha (MIP-1 alpha), MIP-1 beta, and lymphotactin, normally upregulated in the lung during IPS. In contrast, systemic levels of these mediators were unaffected and GVHD-induced lesions in the liver and colon did not differ in severity regardless of ICAM-1 expression. GVHD-mediated mortality was accelerated in ICAM-1(-/-) recipients at doses of allogeneic spleen cells that are otherwise not uniformally lethal. These data implicate ICAM-1 as playing a critical role in the generation of IPS; therefore, ICAM-1 may be a discerning element, segregating IPS from GVHD injury post-alloBMT.
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