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Somatic cell hybrids between human lymphoma lines. III. Surface markers
Author(s) -
Klein George,
Rosén Anders,
Terasaki Paul,
Billing Ron,
Honig Ron,
Jondal Mikael,
Zeuthen Jesper,
Clements Geoffrey
Publication year - 1977
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910190110
Subject(s) - raji cell , beta 2 microglobulin , biology , receptor , surface immunoglobulin , complement system , complement receptor , antibody , microbiology and biotechnology , cell culture , immunology , b cell , genetics
Hybrids between two human lymphoma lines, Raji and Daudi (8A) and Raji and BJAB (83) were examined for genetically determined and/or differentiation‐related surface markers. HL‐A, B cell alloantigens, Fc and complement receptors, EBV receptors and β 2 microglobulin showed an autonomous (“codominant”) expression in the hybrid. This is in contrast to most previous studies on other differentiation markers, involving as a rule crosses between cells of different lineages, where the differentiated pattern usually became “eclipsed” in the hybrid. Staining of activated complement and complement consumption tests showed intermediate or partially suppressed expression in the hybrids. This may be viewed in relation to the fact that these reactions do not merely depend on complement binding to the receptor, but also on subsequent activation and binding of the activated complement. A more complex interaction is also suggested for immunoglobulin production. Surface immunoglobulin showed a suppressive or intermediate pattern in both hybrids, whereas intracellular kappa chain production showed an amplification in the 83 hybrid. The β 2 microglobulin deficiency of the Daudi parent was corrected in the Raji/Daudi hybrid. Two new HL‐A specificities, A10 and BW17, appeared on this hybrid which were not present on the parental lines. This suggests that the HL‐A deficiency of the Daudi cell is due to its lack of β 2 microglobulin.