Brief communication M.J. Herrero M. Bunce M. van Dam zyxwvutsrq R. de Pablo C. Vilches zyxwvutsrq Key words: alloantibodies; 841; Cw*17; HIA-C “blank” Acknowledgments: This work was supported by FIS (Fondo de lnvestigaci6n Sanitaria) grants 95/1603 and 98/ 277. M.J. Herrero was supported by the Fondo de lnvestigacion Sanitaria (grant BAE 97/5025). We thank Martha Messman for help in preparing this manuscript. Received zyxwvutsrqponmlk 29 December 1997, revised. accepted for publication 30 March 1998 Copyrlght (D Munksgaard 1998 nssue Antigens. ISSN 0001-2815 Tissue Antigens 1998: zyxwvutsrqponm 52 92-95 Printed in Denmark. All rights reserved On the nature of “HLA-B41+B42” alloantibodies. Specific reagents for HLACw*l7? zyxw Abstract: An almost complete and bidirectional association exists between HLA-Cw*17 and the HLA-B antigens B41 and B42. Serological and molecular analysis of an individual in which HLA-B*4101 was identified in the ab- sence of Cw*17 provides experimental evidence to prove a previously pro- posed hypothesis predicting that alloantisera classified as %41+B42” are instead specific reagents for HLA-Cw*17. Serological definition of HLA-C polymorphism is poor in compari- son with that of the other classical human MHC class I loci HLA-A and HLA-B. Specific alloantisera, although often weak and crossre- active, are available for the products of the Cw*Ol-Cw*08 alleles. But zyxwvut six additional broad specificities cannot be currently defined by microlymphocytotoxicity and constitute the serological HLA-C “blank” phenotype: Cw*12, Cw*14, Cw*15, Cw*16, Cw*17, and Cw*18 (Cw*13 does not appear to exist) (1, 2). Detection of some of these alleles is possible using broadly reactive HLA-C sera, but their accurate identification is hampered, basically by a lack of mono- specific alloantisera (1, zyxwvu 3-7). The origin of this phenomenon is probably multiple. Firstly, HLA-C molecules are expressed on cell surfaces in lower amounts than HLA-A/Bproteins (8), which could account for occasional fail- ures of alloantisera in recognising cells bearing their nominal HLA- C specificities. However, this does not explain an anecdotal part of serological HLA-C blanks, since reduced expression OCCUTS in both serologically and non-serologically defined alleles (9). Also, the scar- city of individuals apparently sensitized against HLA-C antigens is often attributed to a hypothetical (and never demonstrated) poor immunogenicity,but there are no obvious intrinsic elements in indi- vidual HLA-C alleles which might render them less immunogenic than those of the HLA-A or HLA-B loci. In contrast, some features of HLA-C polymorphism are likely Authon’ al((llatlonr M.J. Herrero‘. M. Bunce2. M. van Dam’, R. de Pablol, C. Vilches’ ‘Servicio de inmunologia. H.U. Clinica Puerta de Hierro. Madrid, Spain, %nspiantation Immunology, Oxford Transplant Centre, Churchill Hospital. Oxford, UK. ’Tissue vping Lab, St. Mary’s Hospital. London, UK Cormopondence to: Carlos Vliches Servicio de Inmunologla H.U. Clinica Puerta de Hierro San Martin de Porres 4 E-28035 Madrid Spain Fax: +34 913160644 Email: cviiches@inmuno.cph.es 92