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The MHC Class I Associated Beta 2 ‐microglobulin (β 2 m) Light Chain is Expressed in a Molar Excess Over HLA‐ABC and CD1 on the Membrane of Leukaemic B Cells but not Leukaemic T Cells: Evidence for Further β 2 m‐Associated Molecules
Author(s) -
JONES R. A.,
CHILD J. A.,
MASTER P. S.,
SCOTT C. S.
Publication year - 1991
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1991.tb01520.x
Subject(s) - cd1 , biology , antigen , microbiology and biotechnology , beta 2 microglobulin , human leukocyte antigen , immunology , cd8 , natural killer t cell
Beta 2 ‐microglobulin (β 2 m) constitutes the common light chain of both the MHC‐encoded HLA‐ABC molecules and a group of structurally related glycoproteins recognized by antibodies of the first cluster of differentiation (CD1a, CD1b and CD1c). These CD1 antigens appear similar to murine T1 and Qa molecules in terms of structure and tissue distribution, although the question of inter‐species homology is controversial. A further group of alloantigens expressed predominantly on T cells has been reported however, with immunogenetic characteristics more closely analogous to the murine T1/Qa system than the CD1 antigens, although their precise identity remains ill‐defined. Having previously shown that malignant B cells may express membrane CD1c, we examined leukaemic B‐cells corresponding to early lymphoblastic differentiation (null‐and common acute lymphoblastic leukaemia) through to the terminal plasma cell stage for the expression of other non‐HLA class I β 2 m ‐associated molecules. It was found that leukaemic B‐cells at intermediate/late stages of differentiation, represented by non‐Hodgkin's lymphoma (B‐NHL) and‘hairy‐cell’leukaemia (HCL), had significantly higher β 2 m: HLA‐ABC ratios than did the cells from other types of B‐cell malignancy. Although leukaemic B cells with a demonstrable non HLA‐ABC‐ associated β 2 m component expressed detectable levels of CD1c. and insignificant levels of CD 1a and CD 1b, the antigen density was insufficient to account for the excess β 2 m. In vitro stimulation of leukaemic B cells by phorbol ester substantially increased the expression of HLA‐ABC and CD1c, but also accentuated further the difference between the expression of these molecules and that of β 2 m. There was no detectable β 2 m other than that associated with HLA‐ABC and CD1 on the surface of malignant T cells by contrast. Our findings strongly support the existence, at certain stages of leukaemic B‐cell differentiation, of an additional β 2 m component(s) other than that associated with HLA‐ABC and CD1.