HLA and malignancy : proceedings of a symposium presented by Roswell Park Memorial Institute, Buffalo, New York, August 19-20, 1976 / editor in chief: Gerald P. Murphy; associate editors: Elias Cohen, John E. Fitzpatrick, David Pressman.

Date:
1977
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Licence: Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)

Credit: HLA and malignancy : proceedings of a symposium presented by Roswell Park Memorial Institute, Buffalo, New York, August 19-20, 1976 / editor in chief: Gerald P. Murphy; associate editors: Elias Cohen, John E. Fitzpatrick, David Pressman. Source: Wellcome Collection.

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    16 / Carpenter et al. which may point to functional as well as to some structural interrelationships. In this regard, it is of interest to note the possibility that another alleUc system linked to HLA, w4, w6 (formerly 4a, 4b) may be the lymphocyte receptor for C3b, the cleaved and activated product of C3 convertase acting upon C3 [51]. The conclusions are based upon the inhibition of EAC rosette formation by alloanti- sera against the w4, w6 system, and suggest that, if not identical to the comple¬ ment receptor, the w4, w6 gene products are at least closely associated with it. The w4, w6 system is clearly independent of HLA-A, B, С loci [8]. In 2 siblings with a variant form of immunodeficiency, HLA antigens and /3-2-microglobulin were lacking from their lymphocytes, yet their cells formed EAC rosettes and reacted with w4, w6 antisera [64]. It has also been shown that human C3 receptors may be closely associated on cell surfaces with a receptor for Epstein-Barr virus [24], although they are not identical structures. Mention should also be made of the Doherty and Zinkernagel hypothesis that мне antigens on cells become modified by viral infection to become the targets for host recognition of and response to the infected cell [12]. Therefore, some important clues are developing which may help to interrelate the whole area of receptors, complement components, and histocompatibility antigens. ACKNOWLEDGMENTS Supported in part by grants from the USPHS AM-11414, AM-05577, RR-05669, AM-5076, Easter Seal Society, New England Peabody Foundation, and the Histocompatibility Research Fund of the Peter Bent Brigham Hospital. REFERENCES L AUen FH, Jr: Linkage of HL-A and GBG. Vox Sang 27:382 (1974). 2. Alper CA, Boneisch T, Watson L: Genetic polymorphism in human glycine-rich beta- glycoprotein. J Exper Med 135:68 (1972). 3. Alper CA, Rosen FS: Genetics of the complement system. In Advances in Human Genetics. In press (1976). 4. Bach FH, Bach ML, Sondel PM, Sheehy MJ, Jarrett-Toth E, Kan C; Assay of HLA-D disparity. Transplant Proceed, in press, (1977). 5. Benacerraf B, McDevitt HD: Histocompatibility-linked immune response genes. Science 175:272 (1972). 6. Bodmer WF, Bodmer JG, Tripp M: Recombination between the LA and 4 loci of the HL-A system. In Histocompatibility Testing, 1970. Copenhagen: Munksgaard, p 187 (1970). 7. Bodmer WF: Report on chromosome 6. In Third International Workshop on Human Gene Mapping, in press (1976). 8. D'Amaro J: w4 (4a) and w6 (4b) in diverse human populations. Demonstration of their genetic identity in population and segregation studies. Tissue Antigens 5:386 (1975).