Quantitative Studies of Antigen Expression in Cultured Murine Lymphoma Cells. II. Cell-Surface Antigens in Synchronized Cultures2

1972 ◽  
Vol 49 (6) ◽  
pp. 1607-1611 ◽  
Author(s):  
Matko Cikes ◽  
Sten Friberg ◽  
George Klein
Keyword(s):  
Cell Surface ◽  
Antigen Expression ◽  
Surface Antigens ◽  
Cell Surface Antigens ◽  
Lymphoma Cells ◽  
Murine Lymphoma ◽  
Quantitative Studies

scholarly journals QUANTITATIVE STUDIES ON THE MIXED LYMPHOCYTE INTERACTION IN RATS

1971 ◽  
Vol 134 (4) ◽  
pp. 857-870 ◽  
Author(s):  
Darcy B. Wilson ◽  
Dianne H. Fox
Keyword(s):  
Cell Surface ◽  
Surface Antigens ◽  
Mouse Cell ◽  
Cell Surface Antigens ◽  
Quantitative Studies ◽  
Lymphocyte Cultures ◽  
Mixed Lymphocyte Cultures ◽  
Environmental Antigens ◽  
Germfree Rats ◽  
Number Of Cells

The proliferative reactivity of lymphocytes from rat donors maintained under germfree or conventional conditions was examined in mixed lymphocyte cultures stimulated with allogeneic and xenogeneic cell surface antigens. The results show (a) that lymphocytes from conventionally maintained rats are less reactive to human, hamster, guinea pig, and mouse cell surface antigens than to the major H alloantigens, and (b) that lymphocytes from germfree rats display no demonstrable reactivity to xenogeneic cells, but are quantitatively normal in their response to allogenic cells. The conclusion drawn from these observations is that the circulating lymphocyte pool of an individual consists of a greater proportion of cells reactive to H alloantigens of other members of the same species than to the xenogeneic cellular antigens of members of other species and that this large number of cells is not generated by a mechanism involving immunization to cross-reactive environmental antigens.

scholarly journals Immunologic classification of lymphocytic leukemias based on monoclonal antibody-defined cell surface antigens

Blood ◽  
1982 ◽  
Vol 59 (2) ◽  
pp. 207-215
Author(s):  
RW Schroff ◽  
KA Foon ◽  
RJ Billing ◽  
JL Fahey
Keyword(s):  
Cell Surface ◽  
B Cell ◽  
Cell Lineage ◽  
Antigen Expression ◽  
Surface Antigens ◽  
Lymphocytic Leukemia ◽  
Leukemic Cells ◽  
Cell Surface Antigens ◽  
Prolymphocytic Leukemia ◽  
Hla Dr

A panel of monoclonal antibodies reactive with normal lymphocyte subsets was used to classify cases of lymphocytic leukemia on the basis of cell surface antigen expression. The antibodies employed were commercially available and included a common framework HLA-DR antibody, two pan-T antibodies (Leu-1 and OKT-3), and antibodies defining cytotoxic/suppressor (Leu-2 and OKT-8) and helper/inducer (Leu-3 and OKT-4) subpopulations of normal T lymphocytes. Cases of ALL could be subgrouped into non-T non-B, pre-T and T-ALL on the basis of reactivity with HLA-DR, Leu-1, and OKT-3 antibodies. Leukemic cells from patients with T-cell CLL could be divided into Leu-2/OKT-8 reactive and Leu- 3/OKT-4 reactive subpopulations, as well as a subgroup in which the majority of cells were unreactive with either of these antibodies. With the exception of one individual, all Sezary cell leukemias expressed a phenotypic pattern similar to that of the Leu-3 subgroup of T-CLL. Malignancies of B-cell lineage (B-CLL, prolymphocytic leukemia, and lymphosarcoma) that were examined were reactive with both the HLA-DR and Leu-1 antibodies. On the contrary, normal B lymphocytes and lymphoid cell lines of B-cell origin did not express surface antigens recognized by the Leu-1 antibody.

scholarly journals Immunologic classification of lymphocytic leukemias based on monoclonal antibody-defined cell surface antigens

Blood ◽  
1982 ◽  
Vol 59 (2) ◽  
pp. 207-215 ◽  
Author(s):  
RW Schroff ◽  
KA Foon ◽  
RJ Billing ◽  
JL Fahey
Keyword(s):  
Cell Surface ◽  
B Cell ◽  
Cell Lineage ◽  
Antigen Expression ◽  
Surface Antigens ◽  
Lymphocytic Leukemia ◽  
Leukemic Cells ◽  
Cell Surface Antigens ◽  
Prolymphocytic Leukemia ◽  
Hla Dr

Abstract A panel of monoclonal antibodies reactive with normal lymphocyte subsets was used to classify cases of lymphocytic leukemia on the basis of cell surface antigen expression. The antibodies employed were commercially available and included a common framework HLA-DR antibody, two pan-T antibodies (Leu-1 and OKT-3), and antibodies defining cytotoxic/suppressor (Leu-2 and OKT-8) and helper/inducer (Leu-3 and OKT-4) subpopulations of normal T lymphocytes. Cases of ALL could be subgrouped into non-T non-B, pre-T and T-ALL on the basis of reactivity with HLA-DR, Leu-1, and OKT-3 antibodies. Leukemic cells from patients with T-cell CLL could be divided into Leu-2/OKT-8 reactive and Leu- 3/OKT-4 reactive subpopulations, as well as a subgroup in which the majority of cells were unreactive with either of these antibodies. With the exception of one individual, all Sezary cell leukemias expressed a phenotypic pattern similar to that of the Leu-3 subgroup of T-CLL. Malignancies of B-cell lineage (B-CLL, prolymphocytic leukemia, and lymphosarcoma) that were examined were reactive with both the HLA-DR and Leu-1 antibodies. On the contrary, normal B lymphocytes and lymphoid cell lines of B-cell origin did not express surface antigens recognized by the Leu-1 antibody.

scholarly journals Immunization of mice with syngeneic Moloney lymphoma cells induces separate antibodies against virion envelope glycoprotein and virus-induced cell surface antigens.

1977 ◽  
Vol 146 (6) ◽  
pp. 1521-1533 ◽  
Author(s):  
E M Fenyo ◽  
E Yefenof ◽  
E Klein ◽  
G Klein
Keyword(s):  
Cell Surface ◽  
Surface Antigens ◽  
Viral Envelope ◽  
Cell Surface Antigens ◽  
Lymphoma Cells ◽  
Test Conditions ◽  
Cell Subline ◽  
Virion Envelope ◽  
Subsequent Staining ◽  
Envelope Antigen

Immunization of mice with heavily irradiated syngeneic Moloney lymphoma cells evokes antibodies against the major viral envelope antigen, gp71, and the Moloney virus-induced cell surface antigen (MCSA). A9HT cells, an L-cell subline, react with the antibodies against the viral envelope antigen only; this reaction can be completely inhibited by virus or purified gp71. Reactivity to Moloney lymphoma cells (YAC) was only partially inhibited (maximum 30%) or not at all. This can be attributed to the reaction of the YAC cells with antibodies directed against MCSA, a nonvirion cell surface component according to both biological and biochemical evidence. Antibody-induced capping of gp71 or p15(E) did not change the membrane distribution of MCSA or H-2, indicating that these antigens represent distinct entities on the cell surface. MCSA showed only minimal capping and thereby differed in behavior from both H-2 and virion antigens. gp71 could be capped by the mouse antiserum as revealed by subsequent staining with monospecific anti-gp71 antiserum. Under ordinary test conditions this reactivity is overshadowed by the reaction against MCSA. The lack of MCSA capping reflects a difference in anchorage of this antigen.

scholarly journals A High-Throughput Hybridoma Selection Method Using Fluorometric Microvolume Assay Technology

2008 ◽  
Vol 13 (3) ◽  
pp. 210-217 ◽  
Author(s):  
Rozanne Lee ◽  
Mylinh Tran ◽  
Mark Nocerini ◽  
Meina Liang
Keyword(s):  
Cell Surface ◽  
High Throughput ◽  
Antigen Expression ◽  
Surface Antigens ◽  
Antibody Binding ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cell Surface Antigens ◽  
Homogeneous Assay ◽  
Exquisite Specificity ◽  
Promising Type

Monoclonal antibodies (mAb) are not only useful reagents but also represent a promising type of therapeutics due to their high affinity and exquisite specificity for their antigens. A critical step in mAb generation is to identify antigen-specific antibodies. Although enzyme-linked immunosorbent assay (ELISA) has been broadly applied for antibody selection against secreted antigens, an inherent disadvantage for ELISA is the difficulty in identifying antibodies that recognize the native conformation of cell surface antigens. To overcome this drawback, the authors have developed a high-throughput cell-based antibody binding assay using fluorometric microvolume assay technology (FMAT). This method offers a homogeneous assay for detection of antibody binding to its antigen on the cell surface. To distinguish antibodies that bind to antigen on the cell surface from those that bind nonspecifically to cells, the binding is assessed using both antigen-expressing cells and related cells devoid of the antigen expression. This assay can detect antibodies at a concentration as low as 5 ng/mL and cell surface antigen as low as 9000 copies per cell. Results demonstrate that the FMAT method provides a sensitive and homogeneous assay to detect antibody binding to cell surface antigens and is amenable for high-throughput hybridoma selection. ( Journal of Biomolecular Screening 2008:210-217)

scholarly journals Anti-Friend virus antibody is associated with recovery from viremia and loss of viral leukemia cell-surface antigens in leukemic mice. Identification of Rfv-3 as a gene locus influencing antibody production.

1979 ◽  
Vol 150 (1) ◽  
pp. 10-19 ◽  
Author(s):  
D Doig ◽  
B Chesebro
Keyword(s):  
Cell Surface ◽  
Genetic Locus ◽  
Leukemia Cell ◽  
Antigen Expression ◽  
Surface Antigens ◽  
Leukemia Cells ◽  
Friend Virus ◽  
Spleen Cells ◽  
Cell Surface Antigens ◽  
Antigen Loss

A single genetic locus, Rfv-3, influenced Friend virus (FV) viremia, loss of FV-induced cell-surface antigens from leukemia cells, and generation of anti-FV antibodies. 30--90 d after FV infection leukemic spleen cells from (B10.A X A)F1 and (B10.A X A.BY)F1 mice (Rfv-3r/s) were found to have low FV-induced cell-surface antigen expression compared to leukemic spleen cells from A and A.BY mice (Rfv-3s/s). In addition, these F1 mice recovered from viremia and generated cytotoxic anti-FV antibodies. A and A.BY mice did not recover from viremia and failed to generate anti-FV antibodies. Anti-FV leukemia cell antibody appeared to mediate FV-antigen loss because decrease of FV cell-surface antigens occurred at the same time as anti-FV antibody appeared in the plasma of F1 mice, and passive transfer of anti-FV antisera induced modulation of FV cell-surface antigens. Rfv-3 did not influence an intrinsic ability of FV antigens to be modulated from Rfv-3s/s leukemia cells because FV antigen loss from Rfv-3s/s spleen cells occurred after transfer of cells to an immune environment.

Expression of myeloid-associated and lymphoid-associated cell-surface antigens in acute myeloid leukemia of childhood: a Pediatric Oncology Group study.

1992 ◽  
Vol 10 (9) ◽  
pp. 1419-1429 ◽  
Author(s):  
S J Kuerbitz ◽  
C I Civin ◽  
J P Krischer ◽  
Y Ravindranath ◽  
C P Steuber ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Cell Surface ◽  
Myeloid Leukemia ◽  
Antigen Expression ◽  
Surface Antigens ◽  
Oncology Group ◽  
Cell Surface Antigens ◽  
Pediatric Oncology Group ◽  
Pediatric Aml ◽  
Acute Myeloid

PURPOSE Although the expression of both myeloid- and lymphoid-associated cell-surface antigens in acute myeloid leukemia (AML) has been described, the clinical significance of such antigen expression remains unknown in the pediatric population. We sought to define an antibody panel for optimal diagnostic antigenic analysis and to test associations among antigen expression and a number of clinical features at presentation and prognosis in pediatric AML. PATIENTS AND METHODS We reviewed the extensive immunophenotypic analysis performed at the time of diagnosis on 132 assessable patients registered on a single Pediatric Oncology Group AML protocol between 1984 and 1988. RESULTS Eighty-eight percent of patients were identified by testing for expression of CD33 and CD13. Overall, 61% of patients expressed at least one lymphoid-associated antigen, most commonly CD4, CD7, or CD19. Expression of CD5, CD10, CD20, or CD22, commonly detected in T- or B-lineage pediatric acute lymphoid leukemia (ALL), was uncommon; coexpression of multiple lymphoid-associated antigens was also uncommon. Expression of the monocyte-associated antigen CD14 correlated with French-American-British (FAB) M4 or M5 morphology. Otherwise, no correlation between antigen expression and FAB classification was noted. None of the myeloid, lymphoid, natural-killer (NK), or progenitor-associated antigens were associated with significant differences in the likelihood of remission induction or event-free survival when expressor versus nonexpressor groups were compared. CONCLUSIONS The distribution of cell-surface antigen expression in pediatric acute leukemia usually permitted the discrimination of AML from ALL by using a limited panel of antibodies. Although the expression of lymphoid-associated antigens was common, such expression did not seem to be associated with an adverse prognosis in pediatric AML.

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