scholarly journals A clone-specific monoclonal antibody that inhibits cytolysis of a cytolytic T cell clone.

1983 ◽  
Vol 157 (3) ◽  
pp. 921-935 ◽  
Author(s):  
D W Lancki ◽  
M I Lorber ◽  
M R Loken ◽  
F W Fitch
Keyword(s):  
Monoclonal Antibody ◽  
T Cell ◽  
Bone Marrow Cells ◽  
Cytotoxic T Lymphocyte ◽  
Cell Clone ◽  
Lymphocyte Culture ◽  
Cytolytic Activity ◽  
Target Cells ◽  
Region Gene ◽  
T Cell Clone

Monoclonal antibody 384.5 specifically inhibited cytolysis of P-815 target cells by cloned L3 cytotoxic T lymphocyte (CTL) effector cells. The lytic activity of other cloned CTL that have other distinct specificities was not affected. Antibody 384.5 did not inhibit the cytolytic activity of bulk populations of C57BL/6 mixed lymphocyte culture (MLC) cells. Concanavalin A-facilitated cytolysis by T cell clone L3 but not T cell clone B18 was inhibited by antibody 384.5, whereas phytohemagglutinin-facilitated cytolysis by L3 cells was not strongly inhibited. Antibody 384.5 binds specifically to L3 cells but not to several other T lymphocytes clones, or to a detectable portion of populations of primary MLC cells, normal spleen, thymus, lymph node, or bone marrow cells. In contrast, C57BL/6 anti-B10.A(5R) secondary MLC cells (genetically enriched for reactivity against the H-2Dd region gene products) contained a small population which reacted with the antibody 384.5. The determinant detected by antibody 384.5 was susceptible to trypsin treatment, and was reexpressed after overnight incubation. These results suggest that the monoclonal antibody 384.5 detects an endogenously synthesized clone-specific determinant associated with the cytolytic activity of the L3 CTL clone. These properties make antibody 384.5 an attractive candidate for an antibody that reacts with the antigen-recognition site of a cytolytic T cell antigen receptor.

scholarly journals A novel type of cell death of lymphocytes induced by a monoclonal antibody without participation of complement.

1995 ◽  
Vol 181 (6) ◽  
pp. 2007-2015 ◽  
Author(s):  
S Matsuoka ◽  
Y Asano ◽  
K Sano ◽  
H Kishimoto ◽  
I Yamashita ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Cell Death ◽  
T Cell ◽  
B Cells ◽  
Interleukin 2 ◽  
Cytolytic Activity ◽  
Target Cells ◽  
T And B Cells ◽  
Fab Fragments ◽  
T Cell Clone

A monoclonal antibody, RE2, raised by immunizing a rat with cell lysate of a mouse T cell clone, was found to directly kill interleukin 2-dependent T cell clones without participation of serum complement. Fab fragments of RE2 had no cytolytic activity, while the cross-linking of Fab fragments with anti-rat immunoglobulin reconstituted the cytotoxicity. The cytotoxicity was temperature dependent: the antibody could kill target cells at 37 degrees C but not at 0 degrees C. Sodium azide, ethylenediaminetetraacetic acid, and forskolin did not affect the cytolytic activity of RE2, while the treatment of target cells with cytochalasin B and D completely blocked the activity. This suggested that the cell death involves a cytoskeleton-dependent active process. Giant holes on the cell membrane were formed within 5 minutes after the treatment with RE2, as observed by scanning electron microscopy. There was no indication of DNA fragmentation nor swelling of mitochondria during the cytolysis, suggesting that the cell death is neither apoptosis nor typical necrosis. The antibody also killed T cell lymphomas and T and B cell hybridomas only when these cells were preactivated with concanavalin A, lipopolysaccharide, or phorbol myristate acetate. Preactivated peripheral T and B cells were sensitive to the cytotoxicity of RE2, while resting T and B cells were insensitive. These results provide evidence for a novel pathway of cell death of activated lymphocytes by membrane excitation.

scholarly journals The natural killer-related receptor for HLA-C expressed on T cells from CD3+ lymphoproliferative disease of granular lymphocytes displays either inhibitory or stimulatory function

Blood ◽  
1996 ◽  
Vol 87 (6) ◽  
pp. 2369-2375 ◽  
Author(s):  
A Cambiaggi ◽  
AM Orengo ◽  
R Meazza ◽  
S Sforzini ◽  
PL Tazzari ◽  
...  
Keyword(s):  
T Cell ◽  
Natural Killer ◽  
Cell Line ◽  
Cell Clone ◽  
Molecular Form ◽  
Lymphoproliferative Disease ◽  
Cytolytic Activity ◽  
Target Cells ◽  
T Cell Clone ◽  
Granular Lymphocytes

Four patients with lymphoproliferative disease of granular lymphocytes (LDGL) coexpressing CD3 and the natural killer (NK)-related “p58” receptor for HLA-C alleles were studied. These CD3+p58+ LDGLs have been detected among a series of 44 CD3+ LDGLs analyzed. Two patients with LDGL (GI and BA) expressed only the p58 molecule defined by the GL-183 and CH-L monoclonal antibodies (MoAbs), while the cases of patients PU and MA also coexpressed the molecular form identified by EB6 anti-p58 MoAb. Three LDGL cases (GI, MA, and PU) displayed the CD8+4-CD16+ T- cell receptor (TCR)alpha/beta+ phenotype, while one patient (BA) was CD8+4+CD16+ TCRalpha/beta+. Freshly isolated granular lymphocytes (GL) from these cases displayed cytolytic activity in an anti-CD3 MoAb- triggered redirected killing assay against the Fcgamma-receptor+ (Fcgamma-R+) P815 target cell line. Lysis of P815 target cells, triggered by an anti-CD3 or by anti-CD16 MoAb, could be inhibited by the addition of anti-p58 MoAb in three fresh or interleukin (IL)-2- cultured GL tested (GI, MA, and PU). Triggering of cytotoxicity against the HLA-DR+ Fcgamma-R+ Daudi cell line induced by appropriate superantigens could also be inhibited by anti-p58 MoAb in patients PU and GI with LDGL. These data indicate that activation through the CD16, CD3, and TCR molecules can be modulated by p58 receptors in these LDGLs. On the contrary, IL-2-expanded cells of patient BA were induced to lyse P815 target cells by anti-p58 MoAb. In addition, anti-p58 MoAB enhanced anti-CD16 MoAb triggered lysis and did not inhibit activation via CD3. These data indicate that, in this particular patient with LDGL, p58 displays a stimulatory effect on cell triggering, rather than the typical inhibitory effect previously observed in p58+ T-cell clones derived from healthy donors. The anti-p58 MoAb did not induce CA++ mobilization in p58+ LDGLs and in a p58+CD3+ normal T-cell clone equipped with inhibitory p58 molecules, while Ca++ mobilization could be observed in cultured GL from patient BA, which could be activated by anti-58 MoAb. These findings suggest that stimulatory and inhibitory p58 molecules are equipped with different signal transducing properties, thus contributing to a better knowledge of the normal counterpart.

Cytotoxicity against lymphoblastoid cells mediated by a T-cell clone from an aplastic anaemia patient: role of CD59 on target cells

1999 ◽  
Vol 107 (4) ◽  
pp. 791-796 ◽  
Author(s):  
Akiyoshi Takami ◽  
Weihua Zeng ◽  
Hongbo Wang ◽  
Tamotsu Matsuda ◽  
Shinji Nakao
Keyword(s):  
T Cell ◽  
Aplastic Anaemia ◽  
Cell Clone ◽  
Target Cells ◽  
Lymphoblastoid Cells ◽  
Patient Role ◽  
T Cell Clone

A monoclonal antibody to an interspecies major histocompatibility determinant inhibits a virus-specific T-cell clone

1982 ◽  
Vol 68 (1) ◽  
pp. 193-198 ◽  
Author(s):  
Michele Allouche ◽  
Jack R. Bennink ◽  
Thomas J. McKearn ◽  
Peter C. Doherty
Keyword(s):  
Monoclonal Antibody ◽  
T Cell ◽  
Cell Clone ◽  
Major Histocompatibility ◽  
T Cell Clone

OKT4 monoclonal antibody-induced activation of an autoreactive T-cell clone

1989 ◽  
Vol 123 (1) ◽  
pp. 244-252 ◽  
Author(s):  
Constantin G. Ioannides ◽  
Ralph S. Freedman ◽  
Chris D. Platsoucas
Keyword(s):  
Monoclonal Antibody ◽  
T Cell ◽  
Cell Clone ◽  
Autoreactive T Cell ◽  
T Cell Clone

Mutated cytochromeb as a determinant of a new monoclonal antibody (H8.98) on renal carcinoma cell lines recognized by a V?3V?1+ T-cell clone

1999 ◽  
Vol 82 (4) ◽  
pp. 562-568 ◽  
Author(s):  
Anita Choudhary ◽  
Robert A. Kurt ◽  
Fran�oise Goret ◽  
Anne Moreau ◽  
Elisabeth Di�z ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
T Cell ◽  
Cell Lines ◽  
Renal Carcinoma ◽  
Carcinoma Cell ◽  
Cell Clone ◽  
Carcinoma Cell Lines ◽  
T Cell Clone

scholarly journals Induction of IgE synthesis in normal human B cells. Sequential requirements for activation by an alloreactive T cell clone and IgE-potentiating factors.

1986 ◽  
Vol 163 (3) ◽  
pp. 713-723 ◽  
Author(s):  
D Y Leung ◽  
M C Young ◽  
N Wood ◽  
R S Geha
Keyword(s):  
T Cell ◽  
B Cells ◽  
Cell Clone ◽  
Mixed Lymphocyte Culture ◽  
Lymphocyte Culture ◽  
T Cell Clones ◽  
Cell Clones ◽  
T Cell Clone ◽  
Ige Synthesis ◽  
Alloreactive T Cell

Two human alloreactive T cell clones were established from a one-way mixed lymphocyte culture involving two nonatopic donors, and were assessed for their capacity to induce IgE synthesis by B cells obtained from the original stimulator. The two alloreactive T cell clones studied induced IgG but not IgE synthesis in normal B cells. However, one of the two clones, clone 2H6, induced IgE synthesis in the presence of supernatants from T cell lines derived from patients with the hyper-IgE syndrome (HIE), and enriched for T cells bearing receptors for IgE. These supernatants by themselves caused no IgE synthesis in nonatopic B cells. The potentiating factors in these supernatants were shown to bind to IgE. Time sequence experiments indicated that interaction of the B cells with the alloreactive clone 2H6 renders them responsive to the action of the IgE-potentiating factors. These results indicate that induction of IgE synthesis in normal B cells involves at least two sequential T cell derived signals. Furthermore, T cell clones are heterogenous in their capacity to provide these signals.

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