Anti-HLA class I antibody binding to airway epithelial cells induces production of fibrogenic growth factors and apoptotic cell death: a possible mechanism for bronchiolitis obliterans syndrome
Section snippets
Abbreviations
- AEC
airway epithelial cell
- BOS
bronchiolitis obliterans syndrome
- BSMC
bronchial smooth muscle cell
- EGF
epidermal growth factor
- HB-EGF
heparin-binding epidermal growth factor
- bFGF
basic fibroblast growth factor
- GM-CSF
granulocyte-monocyte colony-stimulating factor
- IGF
insulin-like growth factor
- mAb
monoclonal antibody
- PDGF
platelet-derived growth factor
- TGF-β
transforming growth factor-β
Cell lines
The KCC-266 AEC line was developed in our laboratory from a lung airway biopsy, immortalized by transfection with the pRSV-Tag plasmid, and cultured in plates precoated with bovine serum albumin, collagen, and fibronectin in LHC-9 medium as previously described [41]. The MRC-5 lung fibroblast cell line was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA) and cultured in RPMI-1640 medium (Gibco BRL, Grand Island, NY, USA) supplemented with fetal bovine serum (15%;
Induction of AEC proliferation by Anti-HLA class I antibodies
We have previously reported that anti-HLA class I antibodies induce tyrosine phosphorylation and proliferation in the A549 lung adenocarcinoma cell line [32]. To determine whether anti-HLA class I antibodies could induce a similar response in a noncancerous AEC line, we incubated KCC-266 AECs in the presence of varying concentrations of the W6/32 mAb (2.5, 5, 10, and 20 μg/ml) for 24 hours. As illustrated in Figure 1, only AECs incubated in the presence of 5 μg/ml of the W6/32 mAb displayed a
Discussion
Previous studies have reported that the development of anti-HLA antibodies after transplantation is associated with chronic rejection in heart and kidney allografts 29, 30. In addition, studies from our laboratory have demonstrated a significant correlation between the development of anti-HLA class I antibodies and the development of BOS after lung transplantation [3]. Furthermore, passive transfer of antidonor MHC class I antibodies has been reported to accelerate the development of cardiac
Acknowledgements
This work was supported by Grants No. HL56643 and HL66452 from the National Institutes of Health. The authors would like to thank Ms. Billie J. Glasscock for secretarial assistance.
References (48)
- et al.
Obliterative bronchiolitis
Clin Chest Med
(1997) - et al.
Indirect allorecognition of mismatched donor HLA class II peptides in lung transplant recipients with bronchiolitis obliterans syndrome
Am J Transpl
(2001) - et al.
Concomitant allorecognition of mismatched donor HLA class I- and II-derived peptides in pediatric lung transplant recipients with bronchiolitis obliterans syndrome
J Heart Lung Transplant
(2003) - et al.
Epithelium-specific adenoviral transfer of a dominant-negative mutant TGF-β type II receptor stimulates embryonic lung branching morphogenesis in culture and potentiates EGF and PDGF-AA
Mech Dev
(1998) - et al.
Chemotaxis of alveolar macrophages in response to signals derived from alveolar epithelial cells
J Lab Clin Med
(1998) - et al.
Expression of GM-CSF receptor and “in vitro” effects of GM-CSF on human fibroblasts
Life Sci
(1998) - et al.
Platelet-derived growth factor-BB, insulin-like growth factor-I, and phorbol ester activate different signaling pathways for stimulation of vascular smooth muscle cell migration
Exp Cell Res
(1998) - et al.
Transforming growth factor-beta (TGF-beta1) genotype and lung allograft fibrosis
J Heart Lung Transplant
(1999) - et al.
Transforming growth factor beta (TGF-β) and obliterative bronchiolitis following pulmonary transplantation
J Heart Lung Transplant
(1999) - et al.
Anti-HLA antibody binding to HLA class I molecules induces proliferation of airway epithelial cellsa potential mechanism for bronchiolitis obliterans syndrome
J Thorac Cardiovasc Surg
(2000)