Cell surface antigens reacting with antiretrovirus sera on normal mouse spleen cells: A flow cytometric study

We retrospectively analyzed the clinicopathological correlation and prognostic value of cell surface antigens expressed by peripheral blood mononuclear cells in patients with mycosis fungoides (MF). 121 consecutive MF patients were included in this study. All patients had peripheral blood flow cytometry as part of their first visit. TNMB and histopathological staging of the cases were retrospectively performed in accordance with International Society for Cutaneous Lymphomas/European Organization of Research and Treatment of Cancer (ISCL/EORTC) criteria at the time of flow cytometry sampling. To determine prognostic value of cell surface antigens, cases were divided into two groups as stable and progressive disease. 17 flow cytometric analyses of 17 parapsoriasis (PP) and 11 analyses of 11 benign erythrodermic patients were included as control groups. Fluorescent labeled monoclonal antibodies were used to detect cell surface antigens: T cells (CD3+, CD4+, CD8+, TCRαβ+, TCRγδ+, CD7+, CD4+CD7+, CD4+CD7−, and CD71+), B cells (HLA-DR+, CD19+, and HLA-DR+CD19+), NKT cells (CD3+CD16+CD56+), and NK cells (CD3−CD16+CD56+). The mean value of all cell surface antigens was not statistically significant between parapsoriasis and MF groups. Along with an increase in cases of MF stage statistically significant difference was found between the mean values of cell surface antigens. Flow cytometric analysis of peripheral blood cell surface antigens in patients with mycosis fungoides may contribute to predicting disease stage and progression.

Download Full-text

Genetic regulation of the antibody response to H-2Db alloantigens in mice. I. Differences in activation of helper T cells in C57BL/10 and BALB/c congenic strains.

Journal of Experimental Medicine ◽

10.1084/jem.141.3.573 ◽

1975 ◽

Vol 141 (3) ◽

pp. 573-583 ◽

Cited By ~ 28

Author(s):

D Wernet ◽

F Lilly

Keyword(s):

T Cell ◽

Cell Surface ◽

Antibody Response ◽

Genetic Regulation ◽

Surface Antigens ◽

T Helper ◽

Spleen Cells ◽

Igg Antibody ◽

Cell Surface Antigens ◽

Helper Function

B10.A(5R) mice immunized with C57BL/10 spleen cells demonstrate a normal T-cell-mediated cytotoxicity to H-2Db tumor cells but they do not mount any IgG antibody response to H-2Db alloantigens. B10.A(5R) mice do show a high titered IgG response when immunized with A.BY cells, which differ at H-2Db plus non-H-2 cell surface antigens, or with B10.A(2R) cells, which differ at H-2Db, H-2Kk, and H-2Ik cell surface antigens. These findings indicate a failure of the T-helper cells to induce the switch from IgM to IgG when the H-2Db alloantigens are the only difference on the immunizing cell. In immunizing H-2d mice with congenic H-g2 cells which differ only in the H-2Db region, mice of the C57BL/10 background made only IgM antibodies whereas mice of the BALB/c background made IgG antibodies. This comparison confirms that genes separate from H-2 regulate the T-cell helper function. The genes that influence the T-cell helper function do not regulate the T-cell-mediated cytotoxicity.

Download Full-text

A NEW SENSITIVE ASSAY FOR ANTIBODY AGAINST CELL SURFACE ANTIGENS BASED ON INHIBITION OF CELL-DEPENDENT ANTIBODY-MEDIATED CYTOTOXICITY

Journal of Experimental Medicine ◽

10.1084/jem.140.5.1348 ◽

1974 ◽

Vol 140 (5) ◽

pp. 1348-1363 ◽

Cited By ~ 28

Author(s):

Phil Halloran ◽

Volker Schirrmacher ◽

Hilliard Festenstein

Keyword(s):

Cell Surface ◽

Surface Antigens ◽

Target Cells ◽

Sensitive Assay ◽

Spleen Cells ◽

Antibody Assay ◽

Cell Surface Antigens ◽

Effector Cells ◽

Cell Antibody ◽

Chicken Erythrocytes

Inhibition of cell-dependent antibody-mediated cytotoxicity has been investigated as a new assay for antibody against cell surface antigens. The cytotoxicity system consisted of effector cells (normal mouse spleen cells), target cells (61Cr-labeled chicken erythrocytes), and antitarget cell antibody. Addition of antibody against cell surface antigens in the effector cell population regularly inhibited the cytotoxicity measured in this system. This cytotoxicity inhibition assay (CIA) detected antibody with a variety of specificities: anti-H-2, anti-Thy 1.2, anti-immunoglobulin, and antimouse bone marrow-derived lymphocyte antigen. When the inhibition by anti-H-2 sera was analyzed using effector cells from congenic mice, the activity was found to be directed against specificities mapping in the H-2K, H-2D, and I regions of the H-2 complex, correlating well with the specificities characterized by complement-dependent assays. A comparison between the sensitivity of the CIA and complement-dependent lysis revealed that the CIA was 2–11 times more sensitive for anti-H-2 antisera and 20–780 times more sensitive for certain antisera against subpopulations of the spleen cells (i.e., T cells or B cells). The CIA proved to be precise, sensitive, and reliable. It may become a very useful antibody assay in various species including man.

Download Full-text

Antibody-induced loss of Friend virus leukemia cell surface antigens occurs during progression of erythroleukemia in F1 mice.

Journal of Experimental Medicine ◽

10.1084/jem.148.5.1109 ◽

1978 ◽

Vol 148 (5) ◽

pp. 1109-1121 ◽

Cited By ~ 9

Author(s):

D Doig ◽

B Chesebro

Keyword(s):

Cell Surface ◽

Leukemia Cell ◽

Surface Antigens ◽

Leukemia Cells ◽

Friend Virus ◽

Spleen Cells ◽

Cell Surface Antigens ◽

Fv Antibody ◽

Quantitative Absorption ◽

Antigen Loss

Friend virus (FV)-induced leukemic spleen cells from (B10.A X A)F1 mice were found to lose sensitivity to antibody-mediated lysis during progression of erythroleukemia. This was correlated with a 78% loss of FV-induced cell surface antigens as determined by quantitative absorption of cytotoxic antibodies and with a decreased percentage of leukemic spleen cells showing membrane immunofluorescence with anti-FV antibody. Antigen loss was observed only with virus-induced antigens, and was limited to antigens expressed on the cell surface. FV-induced antigens were regained when low-antigen leukemia cells from late stages of the leukemia were transferred to lethally irradiated nonimmune recipients, but not when these cells were transferred to hyperimmune lethally irradiated recipients. Conversely, when high-antigen leukemic spleen cells from early stages of the erythroleukemia were transferred to hyperimmune irradiated recipients, antigen loss was induced. The immune response to virus-induced antigens appeared to be involved in causing the antigenic changes observed on leukemia cells in this system.

Download Full-text