scholarly journals 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.

1975 ◽  
Vol 141 (3) ◽  
pp. 573-583 ◽  
Author(s):  
D Wernet ◽  
F Lilly

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.

1976 ◽  
Vol 144 (1) ◽  
pp. 266-271 ◽  
Author(s):  
D Wernet ◽  
F Lilly

B10.A(5R) mice (H-2i5), immunized with spleen cells from congenic B10 mice (H-2b), responded to alloantigens of the H-2Db region by producing antibodies of only IgM type. In contrast, they produced both IgM and IgG antibodies when immunized with noncongenic H-2b cells that carry other foreign cell surface antigens (non-H-2) in addition to H-2Db. A hypothesis was proposed comparing the H-2Db antigen on a congenic cell to a hapten on a nonimmunogenic carrier which fails to induce T-cell helper function responsible for the switch from IgM to IgG secretion in B cells. Data presented here confirmed this hypothesis. 5R mice rendered tolerant to the relevant non-H-2 antigens were unable to mount the anti-H-2Db IgG response in a noncongenic immunization. Tolerance induction did not lead to abrogation of the T-cell mediated cytotoxicity.


1981 ◽  
Vol 78 (6) ◽  
pp. 3858-3862 ◽  
Author(s):  
T. Cotner ◽  
H. Mashimo ◽  
P. C. Kung ◽  
G. Goldstein ◽  
J. L. Strominger

Blood ◽  
1985 ◽  
Vol 66 (5) ◽  
pp. 1115-1123 ◽  
Author(s):  
J Mirro ◽  
TF Zipf ◽  
CH Pui ◽  
G Kitchingman ◽  
D Williams ◽  
...  

Abstract The frequency and clinical significance of acute leukemia displaying both lymphoid and myeloid characteristics was determined in 123 consecutive children using a panel of lineage-associated markers. The leukemic blasts from 18 of 95 children (19%) with the diagnosis of acute lymphoblastic leukemia (ALL) by standard diagnostic criteria expressed myeloid-associated cell surface antigens. Despite immunological evidence of lymphoid differentiation (17 CALLA + and one T cell-associated antigen +) and findings of immunoglobulin gene rearrangement, blasts from these patients reacted with one to five monoclonal antibodies identifying myeloid-associated cell surface antigens (My-1, MCS.2, Mo1, SJ-D1, or 5F1). Dual staining with microsphere-conjugated antibodies and analysis by flow cytometry confirmed that some blasts were simultaneously expressing lymphoid- and myeloid-associated antigens. Conversely, blasts from seven of 28 patients (25%) with acute nonlymphocytic leukemia (ANLL), diagnosed by otherwise standard morphological and cytochemical criteria, expressed lymphoid-associated surface antigens. Dual staining of individual blasts demonstrated simultaneous expression of myeloperoxidase (MPO) (including Auer rods) in association with either T-11, CALLA, or terminal deoxynucleotidyl transferase. Blasts from one patient with ANLL demonstrated T cell receptor gene rearrangement, while blasts from another patient demonstrated characteristics associated with T (T-11), B (CALLA and heavy-chain immunoglobulin gene rearrangement), and myeloid (MPO) lineage. There were no consistent cytogenetic abnormalities, and no patient demonstrated independent leukemic clones. Each patient with typical ALL, except for myeloid-associated antigens, achieved complete remission with conventional induction therapy for ALL. By contrast, three of the seven children with ANLL whose blasts expressed the T-11 surface antigen failed ANLL induction therapy. These three patients subsequently achieved remission with ALL therapy.


2006 ◽  
Vol 366 (1-2) ◽  
pp. 361-362 ◽  
Author(s):  
Yanning Qian ◽  
Qifeng Tang ◽  
Zhongyun Wang ◽  
Jie Sun ◽  
Qi Li

1974 ◽  
Vol 140 (5) ◽  
pp. 1348-1363 ◽  
Author(s):  
Phil Halloran ◽  
Volker Schirrmacher ◽  
Hilliard Festenstein

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.


1978 ◽  
Vol 148 (5) ◽  
pp. 1109-1121 ◽  
Author(s):  
D Doig ◽  
B Chesebro

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.


1979 ◽  
pp. 100-106
Author(s):  
G. J. Hämmerling ◽  
H. Lemke ◽  
U. Hämmerling ◽  
C. Höhmann ◽  
R. Wallich ◽  
...  

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