AbstractA cell line (BS) carrying a variant 11;19 translocation was established following exposure to Epstein-Barr virus (EBV) of the blast cells from an infant with null (B precursor) acute lymphoblastic leukaemia (ALL). Morphology, cytochemistry and immunophenotype were identical to those of the original leukaemic blasts and characteristic of an early B cell neoplasm. Both the cell line and the patient's blasts had an identical karyotype, 46.XY, t(11;19) (q23;p13), t(11;19)(q13;q13). Immunoglobulin heavy chains were rearranged without concomitant light chain rearrangement. No rearrangements of the β, γ or δ chain of the T cell receptor, the proto-oncogene c-ets 1 or the insulin receptor gene which maps to 19p13 were detected. Exposure of the BS line to phorbol ester (PMA) induced a myelomonocytic phenotype with coexpression of B and myeloid cell surface antigens and myeloid cytochemistry. No EBV nuclear antigens (EBNA 1,2) were detectable in the cell line using either immunocytochemical or molecular analyses and the mechanism of “immortalization” by EBV remains unknown. With its unique karyotype, BS provides a useful cell line to study the four translocation breakpoints which occur frequently in both acute lymphoblastic and acute myeloid leukaemias.Key Words: B cell linevariant translocation
A male child presented with recurrent respiratory infections, otitis media, and oral ulceration and was found to be neutropenic. Investigations showed hypogammaglobulinaemia with normal serum IgM and a novel deletion in the gene for CD40 ligand on his X chromosome. Intravenous gammaglobulin did not lead to resolution of his neutropenia; G-CSF was also necessary.
Hybrids formed by fusion of either human acute lymphoblastic or chronic lymphocytic leukemia cells and the mouse myeloma P3.X63.Ag8/653 have been used to show that the expression of two cell surface antigens, Bp37 and p76, associated with B cell activation and detected by the monoclonal antibodies BB1 and BB2, respectively, segregate with human chromosomes 12 and 19, respectively. Another antigen expressed on activated B cells (p24) also maps to chromosome 12 (Katz et al., Eur. J. Immunol. 1984. 13: 1008) which is of interest in the light of the frequent involvement of this chromosome in certain B cell leukemias and lymphomas.
SUMMARY Using anti‐A and anti‐B blood group monoclonal antibodies and fluorescent activated cell sorting of human bone marrow, A (or B) blood group antigen was shown to be on 5.2 ± 5.9 (meanfSD) % of CFU‐GEMM and 12 ± 5 ± 19.6% of the erythroid burst forming cells (designated BFU‐GEMM) as defined by the mixed colony assay, and 49.5±20% of the BFU‐E and 83.5±9.9% of the CFU‐E as defined by the erythroid colony assay. This antigen expression on the BFU‐GEMM is consistent with the concept that erythroid bursts stimulated by leucocyte conditioned medium are less mature, and are closer in development to the pluripotent stem cell than the BFU‐E. These results help to explain the delayed erythropoiesis, and perhaps impaired engraftment of all cell lineages, that may occur in some recipients of ABO incompatible bone marrow transplants, with persistent and high anti‐A titres.
Journal Article Occupational Contact Networks Get access Fred E. Katz Fred E. Katz University of North Carolina Search for other works by this author on: Oxford Academic Google Scholar Social Forces, Volume 37, Issue 1, October 1958, Pages 52–55, https://doi.org/10.2307/2573779 Published: 01 October 1958
The level and avidity of anti-DNA antibody in the serum of New Zealand Black/White (NZB/W F1) hybrid mice has been determined. The results show that there is an age and sex-related variation in the avidity of this antibody. In mice of both sexes, the avidity of circulating anti-DNA antibody increases up to 5 months of age; thereafter the avidity falls with increasing age. These variations are more marked in males, but female mice consistently have lower avidity anti-DNA antibody than males. Thus the time of onset, time course and severity of the murine lupus syndrome in NZB/W F1 mice are associated with the presence of increasing levels of low avidity anti-DNA antibody in the serum. These results are discussed in the context of the possible role of low avidity antibody in immune complex disease.
Beta 2-microglobulin (beta 2m) forms the invariant light chain of the MHC-encoded HLA-ABC and the non-MHC-encoded CD1 molecules. While HLA-ABC (MHC Class I) molecules are virtually ubiquitous in tissue distribution, CD1 determinants by contrast are more restricted. We have assessed, by indirect immunoenzymeassay, the relative membrane densities of these molecules on malignant thymic and post-thymic T cells. It was found that the T cells of mature post-thymic proliferations expressed significantly more beta 2m-associated protein, predominantly HLA-ABC in nature, than thymic-ALL blasts. This parallels the situation found in normal peripheral T cells and thymocytes. In contrast to post-thymic T cells, thymic-ALL blasts showed considerable case to case variation with respect to non-HLA-associated beta 2m and, of particular interest, not all of this excess beta 2m could be accounted for by CD1a. We therefore conclude that other beta 2m-containing molecules may be expressed on thymic-ALL blasts and possibly also on post-thymic leukaemic T cells. In addition, it was found that T cells from CD4+ cases of post-thymic proliferations expressed more beta 2m-associated determinants than other T cells, whether of either normal or malignant origin, and that certain post-thymic malignancies express significantly increased levels of beta 2m-associated protein relative to normal peripheral T-cells. This is in direct contrast to the situation seen in many solid malignancies.
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