T-cell-receptor beta-chain gene rearrangements.
Explore the source record for details and available documents.
Cells, Cultured↗
Biomedical subjects
D M Knowles
Publications and source records attributed to D M Knowles.
A distinctive cutaneous malignant neoplasm expressing the Langerhans cell phenotype. Synchronous occurrence with B-chronic lymphocytic leukemia.
The authors describe a 63-year-old woman who developed a histologically distinctive malignant cutaneous neoplasm composed of large pleomorphic cells with abundant cytoplasm and multilobate, often clefted nuclei that occasionally contained small nucleoli. This neoplastic cell population metastasized to a regional lymph node already involved by a B-cell derived chronic lymphocytic leukemia expressing surface IgMk, BA-1, and OKT1. The large metastatic tumor cells lacked surface immunoglobulin, B-lymphocyte associated antigen BA-1, T-lymphocyte associated antigens OKT1 and OKT3, and the monocyte/macrophage markers lysozyme and alpha 1-antichymotrypsin. These tumor cells expressed HLA-DR antigens, adenosine triphosphatase (ATPase), OKT6, and contained S-100 protein, i.e., they expressed the phenotype peculiar to epidermal Langerhans cells. The typical clinical and histologic features of Histiocytosis X were absent. Thus, this case appears to represent a distinctive cutaneous neoplasm composed entirely of malignant cells of dendritic cell origin which, by immunophenotypic and histochemical analysis, appear to be related to epidermal Langerhans cells.
Antibodies, Monoclonal↗
B-lymphocyte associated differentiation antigen expression by 'non-B, non-T' acute lymphoblastic leukemia.
We investigated the neoplastic cells obtained from 37 cases of 'non-B, non-T' (SIg-E-) acute lymphoblastic leukemia (ALL) for their expression of 13 distinct monoclonal antibody defined B lymphocyte associated differentiation antigens. We correlated the expression of these B cell antigens with terminal deoxynucleotidyl transferase (TdT), HLA-DR antigen, common ALL antigen (cALLa), and cytoplasmic mu heavy chain (Cu) expression by these neoplastic cells. In this way, we were able to describe a hierarchy of B lymphocyte associated differentiation antigens as well as the marked phenotypic heterogeneity of 'non-B, non-T' ALL. TdT and HLA-DR are expressed throughout the stages of B cell differentiation represented by 'non-B, non-T' ALL. The earliest B cell antigen appears to be Leu 12 (B4) followed by BA-2 and then BL2. OKB2, BL1 and BA-1 are acquired next, followed by B1, BL3, cALLa and Cu. BL7 appears just prior to SIg. OKB1, OKB4, OKB7 and BL4 appear at or after the time of SIg expression and hence are not expressed by 'non-B, non-T' ALL cells. This developmental hierarchy is supported by the results of phorbol ester (TPA) induction studies. Thus, cases of 'non-B, non-T' ALL constitute a useful model for probing the hierarchal expression of B cell antigens and delineating the B cell developmental pathway(s).
Antibodies, Monoclonal↗
Monoclonal antibody identification of mononuclear cells in endomyocardial biopsy specimens from a patient with rheumatic carditis.
A 17-year-old woman with rheumatic carditis underwent endomyocardial biopsy both prior to and following treatment with prednisone and aspirin. Frozen sections from the endomyocardial biopsy specimens were studied with monoclonal antibodies by an indirect immunofluorescence technique to define the composition of the inflammatory infiltrate in the myocardium and to determine whether the composition of the infiltrate is distinctive and diagnostically useful. The specimen from the initial biopsy contained a heterogeneous infiltrate composed of T lymphocytes, macrophages, B lymphocytes, and mast cells. T lymphocytes predominated, and the ratio of T-helper to T-cytotoxic/suppressor cells was 2.0. Following treatment the overall cellularity of the infiltrate was diminished, but the infiltrate remained heterogeneous; T cells predominated, and the T-helper to T-cytotoxic/suppressor ratio was reversed, to 0.59. The composition of the inflammatory infiltrate in this case of rheumatic carditis distinguishes it immunologically from other "idiopathic," presumably virus-associated, forms of myocarditis.
Adolescent↗
A membrane protein preferentially expressed by a subpopulation of immature lymphoid cells, epidermal basal keratinocytes, and other epithelial cells.
A murine monoclonal antibody, designated EL-1, was raised by immunization with a human malignant T cell line. It reacted specifically with a membrane antigen expressed on T and B lymphoblastoid cell lines, a subpopulation of normal thymocytes and bone marrow lymphocytes, lymphocytes from a subset of patients with non-B, non-T cell acute lymphoblastic leukemia or T cell acute lymphoblastic leukemia and epithelial stem cells. The latter reactivity was especially striking in the skin, where only basal epidermal keratinocytes and epidermal appendages, including eccrine sweat glands, sebaceous glands and hair follicles, stained positively. A human epidermoid carcinoma cell line was also stained by EL-1. Suprabasilar keratinocytes and acellular keratin did not stain. However, in vitro proliferating fetal lung fibroblasts stained positively. Membrane immunoprecipitation analysis demonstrated that the antigen recognized by antibody EL-1 is a single protein of molecular weight 105 kilodaltons which did not change with exhaustive chemical reduction. Metabolic radiolabeling studies demonstrated that this protein is synthesized by the cell and not merely taken up from the culture medium. This antibody can be useful in studying keratinocyte differentiation in epidermal malignancies and normal skin.
Animals↗
T-cell receptor gene rearrangements as markers of lineage and clonality in T-cell neoplasms.
Ig gene rearrangements represent markers of lineage, clonality, and differentiation of B cells, allowing a molecular diagnosis and immunogenotypic classification of B-cell neoplasms. We sought to apply a similar approach to the study of T-cell populations by analyzing rearrangements of the T-cell receptor beta-chain (T beta) gene. Our analysis, by Southern blotting hybridization using T beta-specific probes of DNAs from polyclonal T cells and from 12 T-cell tumors, indicates that T beta gene rearrangement patterns can be used as markers of (i) lineage, allowing the identification of polyclonal T-cell populations, and (ii) clonality, allowing the detection of monoclonal T-cell tumors. In addition, our data indicate that T beta gene rearrangements represent early and general markers of T-cell differentiation since they are detectable in histologically different tumors at all stages of T-cell development. The ability to determine lineage, clonality, and stage of differentiation has significant implications for future experimental and clinical studies on normal and neoplastic T cells.
Cell Differentiation↗
SIg-E- ("null-cell") non-Hodgkin's lymphomas. Multiparametric determination of their B- or T-cell lineage.
The authors performed immunophenotypic, functional, and molecular analysis of the neoplastic cells from 20 cases of SIg-, E-("null-cell") non-Hodgkin's lymphoma (NHL) in order to determine their lineage, better define this category of NHL, and evaluate the lineage specificity of selected phenotypic markers and the individual and collective utility of these approaches. They assigned 4 cases to the T-cell lineage, and 15 cases to the B-cell lineage, and 1 case remained indeterminant on the basis of immunophenotypic analysis. The cells from 2 cases assigned to the T-cell lineage expressed unusual phenotypes, but their T-cell derivation was confirmed by the demonstration of helper function in vitro. The 15 cases assigned to the B-cell lineage expressed a variety of B-cell-associated antigens, consistent with various stages of B-cell differentiation. Monoclonal antibodies OKT3, OKT4, OKT6, and OKT8 exhibited T-cell lineage restriction; and monoclonal antibodies OKB2, BL1, and B1 exhibited B-cell lineage restriction. Ia, TdT, cALLa, OKT9, and OKT10 exhibited lineage infidelity. Southern blot analysis for immunoglobulin heavy chain gene rearrangements confirmed 18 of the 19 lineage assignments made by immunophenotypic analysis and suggested that the 1 case of indeterminate phenotype was a B-cell neoplasm. One T-cell (OKT3+, T4+) neoplasm exhibited rearranged immunoglobulin heavy chain genes. Thus, neither immunophenotypic analysis nor the demonstration of rearranged immunoglobulin heavy chain genes alone permitted the satisfactory lineage assignment of every case of SIg-, E- NHL. However, combined immunophenotypic, functional, and genotypic analysis allowed us to assign every SIg-, E-NHL to the B- or T-cell lineage and to demonstrate that truly "null-cell" NHLs are probably very uncommon.
Adolescent↗
Alterations in the activity and isozymic profile of human phosphofructokinase during malignant transformation in vivo and in vitro: transformation- and progression-linked discriminants of malignancy.
6-Phosphofructokinase (PFK) plays a central role in the regulation of glycolysis in both normal and neoplastic cells. Since PFK also mediates the Pasteur effect, it coordinates the two modes of energy production in most cell systems, i.e., glycolysis and respiration. The energy production in the cancer cell is characterized by a predominance of aerobic glycolysis (the Warburg effect) and a diminution or lack of the Pasteur effect. Previous studies from this laboratory have demonstrated that PFK in humans and in the rat exists in multiple tetrameric isozymic forms consisting of three unique subunits under separate genetic controls, M, L, and P types. These isozymes are distinguishable from one another by ion-exchange chromatography and subunit-specific antibodies. Various organs exhibit unique isozyme distribution patterns which essentially reflect the preferred mode of carbohydrate metabolism utilized, i.e., glycolysis or gluconeogenesis or both. In order to investigate whether the high aerobic glycolysis of the cancer cell can be explained on the basis of a lack of the regulatory function of PFK due to an altered isozyme distribution pattern, we compared the activity and isozymic profile of the enzyme from malignant cells of human leukemias, lymphomas, virus-transformed cell lines, and established malignant cell lines of lymphoid, myeloid, erythroid, and fibroblastic origin and their normal counterparts. The myeloid and erythroid cell lines were also investigated after in vitro differentiation induced by dimethyl sulfoxide, sodium butyrate, hemin, etc. Our results show that, as is the case with hexokinase and pyruvate kinase, the other two rate-limiting enzymes of glycolysis, PFK shows both quantitative increases and isozymic alterations secondary to altered gene expression during neoplastic transformation, both in vivo and in vitro. In contradistinction to the isozymic alteration in hexokinase and pyruvate kinase, where highly regulated liver-type isozymes decrease or disappear and are replaced by the nonregulated ones, in the case of PFK, the highly regulated liver-type isozyme not only persists but actually increases, followed by an increase in the platelet-type isozyme. These isozymic alterations closely parallel the quantitative increases in total PFK activity, which in turn is closely related to the rate of replication of cancer cells and hence an increase in metabolism. Thus, human PFK is both a transformation- and a progression-linked discriminant of malignancy (For definitions of these terms, see Weber et al., N. Engl. J. Med., 296: 486-493, 1977.).(ABSTRACT TRUNCATED AT 400 WORDS)
Adenosine Triphosphate↗
Monoclonal antibody OKM5 inhibits the in vitro binding of Plasmodium falciparum-infected erythrocytes to monocytes, endothelial, and C32 melanoma cells.
Plasmodium falciparum-infected erythrocytes bind in vitro to human endothelial cells, monocytes, and a certain melanoma cell line. Evidence suggests that this interaction is mediated by similar mechanisms which lead to the sequestration of parasitized erythrocytes in vivo through their attachment to endothelial cells of small blood vessels. We show here that monoclonal antibody OKM5, previously shown to react with the membranes of endothelial cells, monocytes, and platelets, also reacts with the C32 melanoma cell line which also binds P. falciparum-infected erythrocytes. At relatively low concentrations, OKM5 inhibits and reverses the in vitro adherence of infected erythrocytes to target cells. As with monocytes, OKM5 antibody recognizes an 125I-labeled protein of approximately 88 Kd on the surface of C32 melanoma cells. It seems likely, therefore, that the 88 Kd polypeptide plays a role in cytoadherence, possibly as the receptor or part of a receptor for a ligand on the surface of infected erythrocytes.
Antibodies, Monoclonal↗
Leu-M1 antigen expression in T-cell neoplasia.
The Leu-M1 antigen has been recently proposed as a valuable immunodiagnostic marker of the Reed-Sternberg cells of Hodgkin's disease and to be particularly helpful is distinguishing Hodgkin's disease from other lymphoproliferative disorders such as peripheral T-cell lymphomas. In this study, the authors examined paraffin-embedded tissue sections obtained from 38 patients with previously well-characterized T-cell neoplasms for the presence of the Leu-M1 antigen. The cases comprised a spectrum of T-cell malignancies and were divided into four broad clinicopathologic groups: lymphoblastic lymphoma/ leukemias (6), mature T-cell leukemias (3), peripheral T-cell lymphomas (11), and cutaneous T-cell lymphomas (18), which included both mycosis fungoides and nonmycosis fungoides types. The neoplastic T cells in 19 patients (50%) expressed the Leu-M1 antigen. The proportion of Leu-M1-positive cells and the immunostaining pattern varied greatly among these cases but correlated with mature, postthymic stages of T-cell differentiation and activation. Of particular significance was the observation that the more pleomorphic neoplastic T cells, including Reed-Sternberg-like cells, exhibited an intense cytoplasmic and membranous staining pattern which was often indistinguishable from the immunostaining pattern observed in Hodgkin's disease. The authors conclude that Leu-M1 is not a specific immunodiagnostic marker of Hodgkin's disease and has limited value in distinguishing Hodgkin's disease from T-cell neoplasms which stimulate Hodgkin's disease morphologically.
Antibodies, Monoclonal↗
The extranodal lymphoid infiltrate: a diagnostic dilemma.
Lymphoid infiltrates that originate outside of the major lymphoid tissue-bearing sites have often represented a difficult diagnostic problem, and the histopathologic criteria employed to distinguish between benign and malignant extranodal lymphoid infiltrates have not always resulted in accurate prognostication. In part, this has been due to the failure to recognize the existence of primary, extranodal, well-differentiated, small lymphocytic (WDL) lymphoma unassociated with systemic lymphoma or chronic lymphocytic leukemia, the presence of pseudofollicular proliferation centers within WDL lymphoma, and the existence of intermediate differentiated and mantle zone lymphomas that contain residual, atrophic, benign-appearing germinal centers. More recently, the determination of the mono- or polyclonality of extranodal lymphoid infiltrates has given us a new perspective on these lesions. Revisions of the histopathologic criteria and advances in immunology have increased our comprehension of the lymphoid proliferations that originate in the ocular adnexa, skin, lung, and gastrointestinal tract.
Humans↗
Cell marker analysis of extranodal lymphoid infiltrates: to what extent does the determination of mono- or polyclonality resolve the diagnostic dilemma of malignant lymphoma v pseudolymphoma in an extranodal site?
Lymphoid cell marker analysis has provided objective immunologic criteria by which to distinguish between benign pseudolymphomas and malignant lymphomas occurring in extranodal sites and has improved our understanding of extranodal lymphoid proliferations, thereby substantially altering our perspective of these lesions. These studies have resulted in a dramatic reclassification of the majority of the extranodal small lymphocytic proliferations (previously designated pseudolymphomas by histopathologic criteria) as malignant lymphomas, based upon immunologic criteria. However, this redefinition has not truly resolved the diagnostic dilemma of the extranodal small lymphocytic proliferation, nor has it measurably improved our ability to accurately predict patient outcome. It appears that the majority of patients with a monoclonal B small lymphocytic lymphoma localized to a solitary extranodal site enjoy a benign clinical course and long survival with only minimal therapeutic intervention.
B-Lymphocytes↗
T-lymphocyte subpopulations in B-cell-derived non-Hodgkin's lymphomas and Hodgkin's disease.
The authors used E-rosette formation and OKT3 reactivity to determine the percent of T-cells in lymph nodes involved by B-cell non-Hodgkin's lymphomas (B-NHL) and by Hodgkin's disease (HD). The percent of helper and suppressor/cytotoxic T-cells was determined by reactivity with OKT4 and OKT8, respectively. T-cells were also analyzed for two signs of activation: acquisition of Ia antigens and loss of acid a-naphthyl acetate esterase (ANAE) activity. The results were compared with those of lymph nodes exhibiting benign lymphoid hyperplasia (BLH). The percentage of T-cells ranged from 50% to 82%, mean 63 +/- 13%, in 25 cases of BLH, and from 6% to 62%, mean 23 +/- 11%, in 51 cases of B-NHL. The OKT4/T8 ratio was 1.0 to 6.2, mean 3.4 +/- 2.2, in the cases of BLH, and 0.5 to 5.1, mean 2.4 +/- 1.3, in the cases of B-NHL. There was no obvious or significant correlation between the percent of T-cells or the OKT4/T8 ratio and the surface immunoglobulin isotype expressed by the neoplastic B-cells, the morphologic category of B-NHL, or the clinical stage of disease. Activated T-cells were less than or equal to 3% in the cases of BLH and B-NHL. Fifteen lymph nodes involved by HD contained 44% to 96%, mean 74%, E+ (T) cells. Five of these 15 cases contained a significant number of E-OKT3+ cells suggesting that E-rosette formation is not always a reliable T-cell marker in HD. Three other cases contained a large number of E+OKT3- cells. The OKT4/T8 ratio ranged from 0.4 to 21.7, mean 6.7 +/- 5.3, in these cases, representing the most significant T-cell subset imbalances in this series. Large numbers of Ia+E+ and/or E+ANAE- cells, presumably activated T-cells, were present in 7 of these 15 cases of HD. These studies demonstrate the wide variation in the percent of T-cells and in the T-cell subset distribution in lymph nodes exhibiting benign lymphoid hyperplasia and in lymph nodes involved by B-cell-derived non-Hodgkin's lymphomas and Hodgkin's disease.
Antibodies, Monoclonal↗
B- and T-lymphocytes in ocular disease.
Ocular inflammatory diseases and ocular adnexal lymphoid tumors have become less obscure and intimidating by virtue of our ability to study the infiltrates in these various diseases for their B-lymphocyte and T-lymphocyte composition. Comparisons are also possible between lymphocytic profiles in the peripheral blood and the precise composition of the in situ infiltrates within the ocular tissue themselves. The availability of monoclonal antibodies, which can determine T-lymphocytic subsets such as T-helper cells and T-suppressor/cytotoxic cells, natural killer cells, and monocytes-histiocytes, has provided a powerful technology for the delineation of the distinctive immune composition of the inflammatory infiltrates, as well as any possible disturbances in T-cell immunoregulation. B-lymphocytes produce immunoglobulins, which may be misdirected as autoantibodies in local or systemic autoimmune diseases. Immunoglobulin-mediated and therefore B-cell derived conditions include vasculitis, progressive cicatricial ocular pemphigoid, Mooren's corneal ulcer, scleritis, and hay fever and vernal conjunctivitis. Other diseases in which B-lymphocytes, their immunoglobulin products or immune complexes formed with presently unknown antigens are potentially at fault are chronic non-specific uveitis; iridocyclitis in Behcet's syndrome; Fuch's heterochromic syndrome, ankylosing spondylitis, and Reiter's syndrome; Graves' disease; and idiopathic inflammatory orbital pseudotumor and myositis. T-cells do not produce immunoglobins, but rather secrete lymphokines or interact directly with receptors or determinants on viruses or target tissues (eg. immunosurveillance against neoplasia); it is possible that some autoimmune diseases are the result of neo-antigens on the surfaces of host tissues that have been coded for by a cryptic inciting virus. T-cell diseases include phlyctenulosis graft rejections, graft versus host disease, and possibly sympathetic ophthalmia and temporal arteritis. Natural killer cells are involved in many of the same diseases as cytotoxic T-cells, except that the former require no period of sensitization (natural immunity), whereas cytotoxic T-cells must undergo an antigen-specific blast transformation (acquired immunity of the delayed hypersensitivity type). In many diseases in which B-cell derived auto-antibodies are at fault, there may be local tissue or systemic T-cell imbalances, with a reduction in T-suppressor cells and a relative augmentation in T-helper cells, thereby facilitating production of misdirected auto-antibodies.(ABSTRACT TRUNCATED AT 400 WORDS)
Antibodies, Monoclonal↗
Preparation and characterization of monoclonal antibodies recognizing two distinct differentiation antigens (Pro-Im1, Pro-Im2) on early hematopoietic cells.
A series of monoclonal antibodies recognizing myeloid differentiation antigens were prepared by immunizing Balb/c mice with HL-60 cells. Hybrids secreting antibodies reactive with HL-60 cells but unreactive with peripheral blood mononuclear cells were isolated and further cloned. One clone was found to produce an IgG2a antibody recognizing an 85,000-dalton molecular weight surface glycoprotein, and a second clone was found to produce an IgM antibody recognizing a heat-stable determinant present on a glycolipid. We have termed these antigens Pro-Im1 and Pro-Im2, respectively (Pro for using HL-60 promyelocytes as an immunogen and Im for the presence of these antigens on immature cells). alpha Pro-Im1 and alpha Pro-Im2 were used to investigate the surface expression and tissue distribution of these two antigens. Pro-Im1 and Pro-Im2 were found to be brightly expressed on a fraction of fetal liver hematopoietic and bone marrow cells. Both antibodies mediated complement-dependent inhibition of CFU-GM, BFU-E, and CFU-GEMM formation assayed by soft agar colony and burst formation, indicating the expression of these antigens by early hematopoietic precursor cells. This was further confirmed by the induction of HL-60 cells by TPA to differentiate into more mature monocytes and macrophages, accompanied by the loss of both antigens. Pro-Im1 and Pro-Im2 were absent from peripheral blood monocytes, erythrocytes, and platelets, but Pro-Im2 was expressed on granulocytes. Both antigens were absent from thymocytes and peripheral T cells. Cytofluorographic analysis suggested their absence from peripheral blood B cells but that both were expressed on a minority of tissue B cells. Analysis of 150 cases of various myeloid and lymphoid malignancies demonstrated Pro-Im1 and Pro-Im2 expression on myeloblasts and promyelocytes from some acute myelogenous leukemias as well as some B cell malignancies, suggesting that these antigens are shared by early hematopoietic cells and a subset of B cells.
Animals↗
Distribution of antigens defined by OKB monoclonal antibodies on benign and malignant lymphoid cells and on nonlymphoid tissues.
Monoclonal antibodies OKB1, OKB2, OKB4 and OKB7 have been previously shown to detect distinctive antigens displayed on B, but not on T, lymphocytes. Benign and malignant lymphoid cells were investigated for their reactivity with these antibodies in cell suspension by indirect immunofluorescence and in cryostat tissue sections by the avidin-biotin complex immunoperoxidase technique. Fetal liver pre-B cells and pre-B and common type acute lymphoblastic leukemia cells isolated from 15 patients were OKB1-OKB2+OKB4-OKB7-. All mature lymphoid tissue B cells and the neoplastic cell surface immunoglobulin-positive (SIg+) B cells isolated from each of 47 B cell neoplasms were OKB2+. OKB1 and OKB7 were expressed by interfollicular, follicular center, and many, but not all, mantle zone B cells. OKB4 was expressed by follicular center cells, but not by mantle zone or interfollicular B cells. The neoplastic SIg+ B cells isolated from 45 of 47 B cell malignancies were OKB1+OKB4+, and those isolated from 45 of 46 B cell malignancies were OKB7+. The neoplastic B cells of one mantle zone lymphoma were OKB1-, of one small lymphocytic cell lymphoma were OKB7-, of one large cell lymphoma were OKB4-, and of one small lymphocytic cell lymphoma with a monoclonal gammopathy were OKB1-OKB4-. Normal and myeloma plasma cells were OKB-. The malignant T cells isolated from 12 T cell neoplasms were OKB2-OKB4-, but were OKB1+ and/or OKB7+ in 3 cases. Thus, the OKB antibodies appear to detect distinctive antigens that may be expressed at different stages of B cell differentiation. In addition, OKB4 reacted with selected renal and respiratory epithelium, and OKB2 reacted with a wide range of epithelial tissues. The OKB antibodies should prove useful in the investigation of B cell differentiation and may aid in the identification and characterization of lymphoproliferative malignancies with significant therapeutic and prognostic differences not identifiable by conventional histopathologic and immunologic methods.
Animals↗
Preparation and characterization of monoclonal antibodies recognizing three distinct differentiation antigens (BL1, BL2, BL3) on human B lymphocytes.
We report in this paper the generation and characterization of three monoclonal antibodies, designated alpha BL1, alpha BL2, and alpha BL3, that recognize distinctive antigens unrelated to complement, Fc, and mouse erythrocyte rosette receptors, which are preferentially expressed on B lymphocytes. alpha BL1 recognizes a heat stable nonimmunoprecipitable antigen, possibly glycolipid in nature. Alpha BL2 recognizes a nonreducible single polypeptide with a m.w. of 68,000 that occasionally co-precipitates with a p29,34 complex of HLA-DR antigens. Alpha BL3 recognizes a nonreducible single polypeptide with a m.w. of 105,000 with an acidic pI point. We demonstrated that BL1 is expressed on fetal liver hematopoietic cells, a small subset (5 to 15%) of Ficoll-Hypaque-separated normal bone marrow cells, and on a subpopulation of nonadherent, non-E rosette-forming cells and granulocytes. BL2 is expressed on fetal liver hematopoietic cells, on 3 to 7% of normal bone marrow cells, and on a majority (40 to 70%) of nonadherent, non-E rosette-forming cells with a distinctive pattern similar to that of HLA-DR. BL3 is expressed on a subpopulation of nonadherent, non-E rosette-forming cells, and on occasional cells in the monocyte-enriched adherent cell population. The peak fluorescence for BL2 is substantially higher than that of BL1 and BL3, indicating higher BL2 antigen density. All three antigens are absent from thymocytes and E rosette-positive T cell fractions obtained from various lymphoid tissues. Cellular distribution of the BL antigens on various well-characterized established hematopoietic cell lines, leukemias, and malignant lymphomas, in conjunction with the results of the in vitro activation and TPA-induction experiments, suggest that BL1 is expressed during early developmental stages of B cell differentiation, whereas BL3 is expressed at the later stages. BL2 expression spans immature and mature stages of B cell differentiation, with the exception of mature plasma cells. The alpha BL antibodies described here should prove to be useful in the investigation of B cell differentiation and in the clinical diagnosis of lymphoid neoplasms.
Animals↗
Monoclonal anti-human monocyte antibodies OKM1 and OKM5 possess distinctive tissue distributions including differential reactivity with vascular endothelium.
Explore the source record for details and available documents.
Antibodies, Monoclonal↗