The bacteria(B)--antibody(A)--complement(C) (BAC) rosette method for detecting C3 receptors (R): binding specificity and capping of human peripheral blood lymphocyte C3r.
Explore the source record for details and available documents.
Animals↗
Biomedical subjects
J Cossman
Publications and source records attributed to J Cossman.
Malignant lymphomas: The role of immunologic markers in diagnosis, subclassification, and management.
Explore the source record for details and available documents.
B-Lymphocytes↗
Malignant lymphomas as tumours of the immune system.
Malignant lymphomas have traditionally been classified on solely morphological grounds. With new immunological and cytochemical techniques, it has been possible to characterize normal cells of the T-lymphocyte, B-lymphocyte, and monocyte-macrophage system. Application of these methodologies to malignant lymphomas has established their nature as neoplasms of the immune system. Within the B-lymphocyte system it is possible to identify subpopulations responsible for Burkitt's tumour, follicular (nodular) lymphomas, lymphocytic lymphomas of intermediate differentiation and well differentiated lymphocytic lymphomas. The T-lymphocyte system includes lymphoblastic lymphomas, mycosis fungoides, and Sezary's syndrome. Large-cell lymphomas are diverse, but the majority are tumours of transformed lymphocytes, usually of the B-lymphocyte system. The precise nature of the neoplastic cells of Hodgkin's disease (i.e., Reed-Sternberg cells and their mononuclear counterparts) has not yet been established. Despite previous suggestions of a B-lymphocyte or T-lymphocyte origin, recent studies with in vitro cultivation have strongly suggested derivation from the monocyte-macrophage system.
Antibodies, Neoplasm↗
Thymoma: an immunologic and electron microscopic study.
Ultrastructural features, surface morphology and immunologic surface markers were examined on the cells of three human thymomas. The vast majority of the lymphocytes from the thymomas formed spontaneous rosettes with unsensitized sheep erythrocytes in both cell suspension and frozen tissue section and were, therefore, T cells. In addition to the lymphocytes, epithelial cells and macrophages were observed within the thymomas by transmission electron microscopy. When examined by scanning electron microscopy, most lymphocytes had virtually smooth surfaces, whereas cells believed to be epithelial in origin had surface projections.
Adult↗
Complement receptors: specific detection by molecular complexes.
Immune complexes of BSA-anti BSA (IgG F(ab')2) will activate human complement by the alternate pathway. The C3 bound to these complexes binds to human peripheral blood mononuclear cells which bear complement receptors. This interaction is visualized by fluoresceinated antigen (BSA-FITC) or fluorescein conjugated antisera directed at the C3 component of complement. The assay appears to be more sensitive than the usual IgMEAC rosette technique and correlates well with the rosette method.
Animals↗
Coexistence of two lymphomas with distinctive histologic, ultrastructural, and immunologic features.
The unusual coexistence of two distinct lymphomas in 44-year-old woman is described. Nodular, poorly differentiated lymphocytic lymphoma and diffuse histiocytic lymphoma were present in separate sites and were readily distinguished both histologically and ultrastructurally. In addition, the lymphocytic lymphoma was shown to be derived from complement receptor B lymphocytes of follicular center cell type, whereas the histiocytic lymphoma cells were devoid of complement receptors, receptors for IgG (Fc receptors), and surface immunoglobulin. Despite intensive chemotherapy and radiation therapy, the patient died within eight months of the initial diagnosis. Although histiocytic lymphoma was widely disseminated at autopsy, lymphocytic lymphoma was not found. Presumably the histiocytic lymphoma was refractory to therapy, in contrast to the lymphocytic lymphoma, which was selectively eradicated.
Adult↗
Possible role of Fc receptors on cells infected and transformed by herpesvirus: escape from immune cytolysis.
Receptors for the Fc portion of nonimmune immunoglobulin G were demonstrated on B103 rat brain neuroma cells infected with herpes simplex virus type 1 (HSV-1) KOS by a radioimmunoassay using 125I-labeled heat-aggregated Fc fragments. Immune F(ab')2 fragments specific for HSV antigens competed efficiently for Fc binding sites, suggesting that the binding of Fc fragments to infected cells is specific for viral cell-surface antigens. It has been suggested that the binding of immune complexes to Fc receptors on the surfaces of tumor cells in vivo plays a role in protecting these cells from immune destruction. In vitro evidence is presented for the ability of aggregated immunoglobulin G molecules bound to cell-surface Fc receptors to protect both HSV-infected and HSV-transformed cells against complement-dependent and cell-mediated immune lysis.
Animals↗
Complement receptor B lymphocytes in nodular sclerosing Hodgkin's disease.
Infiltrated tissues from nine cases of nodular sclerosing Hodgkin's disease (NSHD) were examined for immunologic cell surface markers. In all nine cases a large population of complement receptor B-lymphocytes were present within the nodular infiltrates. B-lymphocytes were identified in frozen sections by adherence of sheep red blood cells (E) coated with IgM antibody (A) and complement (C) IgMEAC). IgMEAC attached to both small lymphocytes and to Reed-Sternberg cells and their variants. Red cells coated with IgG (IgGEA) attached to histiocytes associated with the internodular fibrous bands and only sparsely with the nodular infiltrates. The population of complement receptor lymphocytes appears to be an integral component of NSHD.
Adult↗
Immunologic surface markers in non-Hodgkin's lymphomas.
Tissues from 21 patients with non-Hodgkin's lymphomas were examined for immunologic cell surface markers. Patterns of distribution of complement receptor (CR) B lymphocytes and Fc receptor (FcR)-bearing histiocytes in tumor tissue were evaluated and compared to routine histologic preparations of the tumors and to normal tissue. The lymphomatous infiltrates from all 6 cases of nodular, poorly differentiated lymphocytic lymphoma (NPDLL) consisted of dense populations of CR B lymphocytes. Involved tissue from 7 of 8 patients with diffuse, poorly differentiated lymphocytic lymphoma (DPDLL) was predominately comprised of CR B lymphocytes. Discrete nodules of CR B cells were present in a lymph node replaced by DPDLL. FcR were identified on the cells from 1 of 3 cases of histiocytic lymphoma. None of the 4 cases of undifferentiated lymphoma possessed demonstrable surface markers in tissue section; however, the cell suspension from 1 case contained a high percentage of CR B cells. Both CR and T cell markers were present on the cells of DPDLL of childhood.
Adult↗
Warthin tumor. B-lymphocytes within the lymphoid infiltrate.
The lymphoid stroma in Warthin tumor is predominantly composed of complement receptor B-lymphocytes. These lymphocytes are present in a pattern similar to that observed in reactive lymph nodes. The B-lymphocytes may be residual lymph node elements exhibiting reactivity directed toward the epithelial component of the tumor.
Adenolymphoma↗
Hairy cell leukemia. An immunologic and ultrastructural study.
A case of hairy cell leukemia in a 39-year-old man is reported. Hairy cells from the peripheral blood, spleen, and bone marrow had lambda-type immunoglobulin on their surfaces; those from the peripheral blood and bone marrow also had IgD on their cell membranes. Frozen sections of spleen reacted with IgGEA, but not IgMEA or IgMEAC markers. Transmission electron microscopy revealed ribosome-lamella complexes in cells from the spleen, but not the peripheral blood. Scanning electron microscopy demonstrated a spectrum of cell surface morphology with many cells characterized by ridges and ruffles. The significance of these findings is considered and it is suggested that the hairy cell is a B lymphocyte.
Adult↗
Detection of antigens similar to placental antigens in mouse fertilized eggs by immunofluorescence.
Explore the source record for details and available documents.
Animals↗
Secular trend in neonatal mortality in the moutain states.
Explore the source record for details and available documents.
Altitude↗
Rearranging antigen-receptor genes in enriched Reed-Sternberg cell fractions of Hodgkin's disease.
Molecular genetic analysis of rearranging antigen-receptor genes in non-Hodgkin's lymphomas has revealed the clonality and lineage in the majority of cases. In an analogous approach, we sought to apply gene rearrangement analysis to Hodgkin's disease to understand better the clonality and origin of this disorder. However, the putative neoplastic cell of Hodgkin's disease, the Reed-Sternberg cell and its variants, is extraordinarily rare in most cases of Hodgkin's disease. On the average, Reed-Sternberg cells and variants represent 0.1 per cent of total cell suspensions of nodular sclerosing Hodgkin's disease. As this frequency is below the minimum threshold of sensitivity of the Southern blot assay, we attempted to enrich for Reed-Sternberg cells before DNA extraction and analysis. Using either elutrition or Percoll density gradient centrifugation, we were able to enrich the percentage of Reed-Sternberg cells and variants to above 1 per cent in five cases of nodular sclerosing Hodgkin's disease. In three of these cases, immunoglobulin gene rearrangements were identified, but no T cell receptor gene rearrangements were seen. No rearrangements were detected in unseparated cells or in the Reed-Sternberg cell-depleted fractions. In addition, the L428 Hodgkin's disease cell line was found to have one rearranged and one deleted heavy-chain gene, a rearranged kappa gene, a rearranged lambda gene, and a single rearranged beta allele. No rearrangements of the T gamma gene were found in L428. Taken together, these findings indicate that clonal cell populations are present in Hodgkin's disease and suggest the possibility of a clonally expanded lymphoid cell in this disorder.
Genes, Immunoglobulin↗
Isolation of HTLV-transformed B-lymphocyte clone from a patient with HTLV-associated adult T-cell leukaemia.
The human T-cell leukaemia/lymphoma virus (HTLV) is an exogenous retrovirus which has been associated with adult T-cell leukaemia/lymphoma (ATL). This malignancy of T lymphocytes is endemic to southern Japan, the West Indies, and to a lesser extent, the Middle East, Central Africa and the southeastern United States. ATL cells from patients of diverse geographical origins have been found to be infected with HTLV-1 (ref.6). HTLV is normally tropic for mature T lymphocytes, especially those expressing the helper-inducer surface antigen phenotype (OKT4 or Leu-3-positive), and the neoplastic T cells infected with HTLV generally express receptors for T-cell growth factor (detected by reactivity with anti-Tac antibody). However, we report here the isolation of a HTLV-infected B-lymphocyte clone from the peripheral blood of a patient with ATL. This clone is cytogenetically normal and is not infected with Epstein-Barr virus (EBV). Co-culture of cells from this clone with cord blood lymphocytes resulted in transmission of HTLV and the immortalization of either T or B lymphocytes. These results suggest that HTLV may be associated with a broader range of host cells than previously recognized.
Antigens, Surface↗
Clustering of breakpoints on chromosome 11 in human B-cell neoplasms with the t(11;14) chromosome translocation.
The t(11;14) (q13;q32) chromosome translocation has been reported in diffuse small and large cell lymphomas and in chronic lymphocytic leukaemia (B-CLL) and multiple myeloma. Because chromosome band 14q32 is involved in this translocation, as well as in the t(8;14) (q24;q32) translocation of the Burkitt tumour, interruption of the immunoglobulin heavy-chain locus was postulated for this rearrangement. We have cloned the chromosomal joinings between chromosomes 11 and 14 and also between chromosomes 14 and 18, in B-cell tumours carrying translocations involving these chromosomes, and suggested the existence of two translocated loci, bcl-1 and bcl-2, normally located on chromosomes 11 (band q13) and 18 (band q21) respectively, involved in the pathogenesis of human B-cell neoplasms. The results indicate that in the leukaemic cells from two different cases of CLL, the breakpoints on chromosome 11 are within 8 nucleotides of each other and on chromosome 14 involve the J4-DNA segment. Because we detected a 7mer-9mer signal-like sequence with a 12-base-long spacer on the normal chromosome 11, close to the breakpoint, we speculate that the t(11;14) chromosome translocation in CLL may be sequence specific and may involve the recombination system for immunoglobulin gene segment (V-D-J) joining.
B-Lymphocytes↗