Summary.-The lymphocyte marker pattern of non-Hodgkin's lymphoma cells was related to current concepts of lymphoma classification. In a series of 28 lymphomas, lymphocyte markers indicated that 2 were of histiocytic origin, 2 were unclassifiable, none were derived from T cells and the remainder were B -cell neoplasms. The immunoglobulin heavy chain associated with the B-cell tumours was y in one case, af in one case but was ,-in the majority of cases, reflecting the predominance of this heavy chain, together with 8 chains, on normal lymph node lymphocytes in man. 8 chains accompanied ,u chains on the tumour cells i!1 6/17 lymphomas in which anti-8 staining was performed. 8 chains were not found on any lymphomas other than well differentiated diffuse lymphocytic types. There was evidence of a reduction in surface immunoglobulin, Fcy and C3 receptors on undifferentiated lymphoma cells. T lymphocytes of normal morphology were present in all lymphomas except one, and were more numerous in follicular lymphomas than in diffuse tumours.
This report describes the phenotypic analysis of a cell line obtained from a female patient with the nodular sclerosing subtype of Hodgkin's disease (HD). The cell line has a neoplastic karyotype and is stable in culture in the absence of feeder layers or growth factors. Phenotypic analysis of this cell line shows that it cannot easily be characterized as either a lymphocyte, macrophage or granulocyte but resembles in its characteristics certain HD lines already described in the literature. The cell line carries the antigen defined by the Ki-1 monoclonal antibody, shows myeloid markers on a proportion of cells and has cytoplasmic UCH-T1.
SUMMARY In an immunohistochemical study of 26 biopsies from 24 patients with Hodgkin's disease a granular staining pattern for alpha-l-antitrypsin (ct,AT) and alpha-l-antichymotrypsin (a,ACT) was seen in Reed-Sternberg (RS)
The graft-vs-host reaction (GVHR) generated by the injection of parental lymphocytes into unirradiated immune-competent F1 hosts is characterized by an acute loss of immune functions, an attack on host tissues, and a gradual recovery of function. Flow cytometric analysis of the donor- and host-derived splenic populations during the course of acute dysfunction and gradual recovery revealed a complex pattern of changes in lymphoid and myeloid populations that resulted in the repopulation of the host with donor-derived cells. Initially, donor-derived T cell populations expanded, particularly CD8+ T cells. Next, host T cell and B cell populations disappeared. Finally, donor-derived cells repopulated the lymphohematopoietic system in the sequence myeloid populations, B cells, and, after a protracted period, T cells. The recovery of immune functions following GVHR-induced immune deficiency was associated with this repopulation of the spleen by donor-derived cells. Donor repopulation of the host lymphohematopoietic system required the presence of both CD4 and CD8 cells in the original donor inoculum. Depletion of donor CD4 populations precluded development of GVHR or any donor engraftment; depletion of CD8 cells resulted in engraftment solely of donor CD4 populations.
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