THE APPLICATION OF HUMAN MONOCLONAL-ANTIBODIES FOR MONITORING DONOR DERIVED SOLUBLE HLA CLASS-I MOLECULES IN THE SERUM OF HEART-TRANSPLANT RECIPIENTS

Citation
Ca. Koelman et al., THE APPLICATION OF HUMAN MONOCLONAL-ANTIBODIES FOR MONITORING DONOR DERIVED SOLUBLE HLA CLASS-I MOLECULES IN THE SERUM OF HEART-TRANSPLANT RECIPIENTS, Human immunology, 59(2), 1998, pp. 106-114
Citations number
47
Categorie Soggetti
Immunology
Journal title
ISSN journal
01988859
Volume
59
Issue
2
Year of publication
1998
Pages
106 - 114
Database
ISI
SICI code
0198-8859(1998)59:2<106:TAOHMF>2.0.ZU;2-B
Abstract
Increased levels of both donor and recipient derived HLA molecules can be found in serum and plasma of transplanted patients during rejectio n. Recent data suggest that levels of donor specific soluble HLA Class I (sHLA-1) correlate better with graft rejection than total sHLA Clas s I [1, 2]. Therefore, quantification of donor specific soluble counte rparts of HLA Class I in the serum of the recipient may be a new way f or non-invasive monitoring of rejection after organ transplantation. U p to now, only a limited number of mouse monoclonal antibodies (alpha HLA-A2,and alpha HLA-B7) has been used in enzyme linked immunosorbent assays (ELISAs) io detect donor specific HLA molecules in the plasma o f transplant recipients. To monitor other donor-recipient combinations , we tested some of our HLA Class I specific human monoclonal antibodi es, routinely used in complement-dependent cytotoxicity, for their sui tability in ELISA based assays. In the present model system, we used a lpha HLA-A9 (BvK5C4) or alpha HLA-A3 (OK2F3) hybridoma-supernatant to set up a sHLA-A9 and sHLA-A3 specific ELISA. In a pilot study we show that these assays were sensitive enough re detect an increase of donor specific sHLA-I during rejection in the plasma of two heart transplan t recipients. Use of a large set of human hybridoma's will enable moni toring most recipient/donor combinations in the near future. (C) Ameri can Society for Histocompatibility and Immunogenetics, 1998. Published by Elsevier Science Inc.