Allogeneic bronchoalveolar lavage cells induce the histology and immunology of lung allograft rejection in recipient murine lungs - Role of intercellular adhesion molecule-1 on donor cells

Citation
Ds. Wilkes et al., Allogeneic bronchoalveolar lavage cells induce the histology and immunology of lung allograft rejection in recipient murine lungs - Role of intercellular adhesion molecule-1 on donor cells, TRANSPLANT, 67(6), 1999, pp. 890-896
Citations number
42
Categorie Soggetti
Medical Research Diagnosis & Treatment
Journal title
TRANSPLANTATION
ISSN journal
00411337 → ACNP
Volume
67
Issue
6
Year of publication
1999
Pages
890 - 896
Database
ISI
SICI code
0041-1337(19990327)67:6<890:ABLCIT>2.0.ZU;2-2
Abstract
Background, Intercellular adhesion molecule (ICAM)-1 expressed on accessory cells has a key role in antigen presentation. The histology and immunology of lung allograft rejection is postulated to result from donor lung access ory cells presenting alloantigens to recipient lymphocytes, and, therefore, ICAM-1 may have a crucial role in the rejection process. We have previousl y reported that the instillation of allogeneic (C57BL/6, I-ab) bronchoalveo lar lavage (BAL) cells (96% macrophages, 2% dendritic cells) into the lungs of recipient BALB/c mice (I-ad) induced the histology and immunology of ac ute lung allograft rejection. Using this model, the purpose of the current study was to determine the role of ICAM-1 on donor lung cells in lung allog raft rejection, Methods. BALB/c mice received allogeneic BAL cells from wild-type or ICAM-1 mutant (lacking ICAM-1 expression) C57BL/6 mice by nasal insufflation week ly for 4 weeks. Recipient mice underwent BAI, and serum collection for the determination of T helper 1/T helper 2 cytokines and IgG subtypes, Lung his tology was graded using standard criteria for allograft rejection. Results. Although wild-type cells induced a lymphocytic vasculitis and bron chitis, ICAM-1 mutant allogeneic BAL cells only induced a lymphocytic vascu litis in recipient lungs. Both wild-type and ICAM-1 mutant cells induced up -regulated local interferon-gamma and IgG2a production, and deposition of I gG2a in recipient lungs. Conclusions. These data show that ICAM-1 on donor lung accessory cells medi ates differential effects on the histology and immunology of acute lung all ograft rejection.