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Bronchiolitis obliterans syndrome due to donor-specific HLA-antibodies.
Tissue Antigens. 2015 Sep; 86(3):178-85.TA

Abstract

Chronic lung allograft dysfunction (CLAD) is a limiting factor for long-term survival in lung transplant recipients. Donor-specific human leukocyte antigen (HLA)-antibodies (DSA) have been suggested as potential risk factors for CLAD. However, their impact on clinical outcome following lung transplantation remains controversial. We performed a single-center study of 120 lung transplant recipients transplanted between 2006 and 2011. Patient sera were investigated before and after transplantation. The sera were screened by means of Luminex(®) technology (Luminex Inc., Austin, TX, USA) for IgG-HLA-class I and class II antibodies (ab). Using single antigen beads, DSA were identified and correlated retrospectively with clinical parameters. After transplantation 39 out of 120 patients (32.5%) were positive for HLA-ab. The incidence of de novo DSA formation was 27 of 120 patients (22.5%). Eleven of 27 (41%) of de novo DSA-positive patients developed BOS compared to 13 of 93 (14%) DSA-negative patients (p = 0.002). Furthermore, the generation of de novo DSA was independently associated with the development of BOS in multivariable analysis [hazard ration (HR) 2.5, 95% confidence interval (CI) 1.0-6.08; p = 0.046). Our results indicate that de novo DSA are associated with the development of BOS after lung transplantation. Monitoring of HLA-ab after transplantation is useful for identifying high-risk patients and offers an opportunity for early therapeutic intervention.

Authors+Show Affiliations

Laboratory for Immunogenetics, University Hospital Grosshadern, Ludwig-Maximilians-University, Munich, Germany. Department of General, Visceral, Transplantation, Vascular and Thoracic Surgery, University Hospital Grosshadern, Ludwig-Maximilians-University, Munich, Germany.Department of Internal Medicine V, University Hospital Grosshadern, Ludwig-Maximilians-University, and Asklepios Fachkliniken München-Gauting, Comprehensive Pneumology Center Munich (CPC-M), Member of the German Center for Lung Research (DZL), Munich, Germany.Department of Internal Medicine V, University Hospital Grosshadern, Ludwig-Maximilians-University, and Asklepios Fachkliniken München-Gauting, Comprehensive Pneumology Center Munich (CPC-M), Member of the German Center for Lung Research (DZL), Munich, Germany.Laboratory for Immunogenetics, University Hospital Grosshadern, Ludwig-Maximilians-University, Munich, Germany.Department of General, Visceral, Transplantation, Vascular and Thoracic Surgery, University Hospital Grosshadern, Ludwig-Maximilians-University, Munich, Germany.Department of Cardiac Surgery, University Hospital Grosshadern, Ludwig-Maximilians-University, Munich, Germany.Department of General, Visceral, Transplantation, Vascular and Thoracic Surgery, University Hospital Grosshadern, Ludwig-Maximilians-University, Munich, Germany.Department of General, Visceral, Transplantation, Vascular and Thoracic Surgery, University Hospital Grosshadern, Ludwig-Maximilians-University, Munich, Germany.Comprehensive Pneumology Center Munich (CPC-M), Institute of Lung Biology and Disease, Helmholtz Zentrum München, Member of the German Center for Lung Research (DZL), Munich, Germany.Department of Anaesthesiology, University Hospital Grosshadern, Ludwig-Maximilians-University, Munich Lung Transplant Group (MLTP), Munich, Germany.Department of Internal Medicine V, University Hospital Grosshadern, Ludwig-Maximilians-University, and Asklepios Fachkliniken München-Gauting, Comprehensive Pneumology Center Munich (CPC-M), Member of the German Center for Lung Research (DZL), Munich, Germany.Department of General, Visceral, Transplantation, Vascular and Thoracic Surgery, University Hospital Grosshadern, Ludwig-Maximilians-University, Munich, Germany.Department of Internal Medicine V, University Hospital Grosshadern, Ludwig-Maximilians-University, and Asklepios Fachkliniken München-Gauting, Comprehensive Pneumology Center Munich (CPC-M), Member of the German Center for Lung Research (DZL), Munich, Germany.Department of General, Visceral, Transplantation, Vascular and Thoracic Surgery, University Hospital Grosshadern, Ludwig-Maximilians-University, Munich, Germany.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

26204790

Citation

Kauke, T, et al. "Bronchiolitis Obliterans Syndrome Due to Donor-specific HLA-antibodies." Tissue Antigens, vol. 86, no. 3, 2015, pp. 178-85.
Kauke T, Kneidinger N, Martin B, et al. Bronchiolitis obliterans syndrome due to donor-specific HLA-antibodies. Tissue Antigens. 2015;86(3):178-85.
Kauke, T., Kneidinger, N., Martin, B., Dick, A., Schneider, C., Schramm, R., Meimarakis, G., Preissler, G., Eickelberg, O., von Dossow, V., Behr, J., Hatz, R., Neurohr, C., & Winter, H. (2015). Bronchiolitis obliterans syndrome due to donor-specific HLA-antibodies. Tissue Antigens, 86(3), 178-85. https://doi.org/10.1111/tan.12626
Kauke T, et al. Bronchiolitis Obliterans Syndrome Due to Donor-specific HLA-antibodies. Tissue Antigens. 2015;86(3):178-85. PubMed PMID: 26204790.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Bronchiolitis obliterans syndrome due to donor-specific HLA-antibodies. AU - Kauke,T, AU - Kneidinger,N, AU - Martin,B, AU - Dick,A, AU - Schneider,C, AU - Schramm,R, AU - Meimarakis,G, AU - Preissler,G, AU - Eickelberg,O, AU - von Dossow,V, AU - Behr,J, AU - Hatz,R, AU - Neurohr,C, AU - Winter,H, Y1 - 2015/07/23/ PY - 2015/03/14/received PY - 2015/06/13/revised PY - 2015/06/27/accepted PY - 2015/7/25/entrez PY - 2015/7/25/pubmed PY - 2016/5/10/medline KW - bronchiolitis obliterans syndrome KW - chronic lung allograft dysfunction KW - human leukocyte antigen-antibodies KW - humoral rejection KW - lung transplantation SP - 178 EP - 85 JF - Tissue antigens JO - Tissue Antigens VL - 86 IS - 3 N2 - Chronic lung allograft dysfunction (CLAD) is a limiting factor for long-term survival in lung transplant recipients. Donor-specific human leukocyte antigen (HLA)-antibodies (DSA) have been suggested as potential risk factors for CLAD. However, their impact on clinical outcome following lung transplantation remains controversial. We performed a single-center study of 120 lung transplant recipients transplanted between 2006 and 2011. Patient sera were investigated before and after transplantation. The sera were screened by means of Luminex(®) technology (Luminex Inc., Austin, TX, USA) for IgG-HLA-class I and class II antibodies (ab). Using single antigen beads, DSA were identified and correlated retrospectively with clinical parameters. After transplantation 39 out of 120 patients (32.5%) were positive for HLA-ab. The incidence of de novo DSA formation was 27 of 120 patients (22.5%). Eleven of 27 (41%) of de novo DSA-positive patients developed BOS compared to 13 of 93 (14%) DSA-negative patients (p = 0.002). Furthermore, the generation of de novo DSA was independently associated with the development of BOS in multivariable analysis [hazard ration (HR) 2.5, 95% confidence interval (CI) 1.0-6.08; p = 0.046). Our results indicate that de novo DSA are associated with the development of BOS after lung transplantation. Monitoring of HLA-ab after transplantation is useful for identifying high-risk patients and offers an opportunity for early therapeutic intervention. SN - 1399-0039 UR - https://www.unboundmedicine.com/medline/citation/26204790/Bronchiolitis_obliterans_syndrome_due_to_donor_specific_HLA_antibodies_ L2 - https://doi.org/10.1111/tan.12626 DB - PRIME DP - Unbound Medicine ER -