A monoclonal antibody (RH1-38) which inhibits multiple systems of cell-mediated cytotoxicity—II. Evidence that the epitope recognized is involved in a late step in the cytolytic mechanism

Hall, Robert E.; Schall, Rebecca P.; Black, Laura A.

doi:10.1016/0161-5890(85)90141-5

Cited by 10 publications

(2 citation statements)

References 24 publications

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“…Several groups have shown that marked inhibition of NK-mediated cytolysis is induced by anti-LFA-1-e (CDlla) and anti-LFA-l-,B (CD18) MAbs; these findings strongly suggest such surface molecules play important roles in NK-mediated cytolysis (Hall et al, 1985;Schmidt et al, 1985). In addition, it has been found that ICAM-1 appears to be constitutively avid for LFA-1.…”

Section: Discussionmentioning

confidence: 96%

Tumour necrosis factor-α induces an increase in susceptibility of human glioblastoma U87-MG cells to natural killer cell-mediated lysis

Kondo

Yin²,

Takeuchi³

et al. 1994

Br J Cancer

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Section: Discussionmentioning

confidence: 96%

Tumour necrosis factor-α induces an increase in susceptibility of human glioblastoma U87-MG cells to natural killer cell-mediated lysis

Kondo

Yin²,

Takeuchi³

et al. 1994

Br J Cancer

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“…Contacts between effector cells and target cells are mediated by specific receptors and accessory surface adhesion molecules. Adhesion molecules such as CD2, CD 11 a/CD 18 (Leukocyte function-associated antigen, LFA-1) CD lib/CD 18 (Mac-1), and CD54 (intercellular adhesion molecule, ICAM-1) have important roles in NK cell-mediated cytolysis (2,3). However, the adhesion molecules involved in virus-infected cell killing mediated by NK cells have not been fully characterized.…”

Section: Natural Killer (Nk) Cells Lyse Tumor Cells or Virus-infectedmentioning

confidence: 99%

Role of Adhesion Molecules in Natural Killer Cell-Induced DNA Fragmentation of Cytomegalovirus-Infected Fibroblasts

Ito

Watanabe²,

Kamiya³

et al. 1996

Viral Immunology

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We investigated the roles of CD11a, CD11b, CD18, and CD54 adhesion molecules in non-adherent peripheral blood mononuclear cells (NPBMC)-induced DNA fragmentation of cytomegalovirus (CMV)-infected cells. DNA fragmentation in the supernatant from CMV-infected cells and NPBMC was assayed, and cytotoxicity against CMV-infected cells was calculated. Treatment of NPBMC with monoclonal antibodies to CD11a, CD11b, CD18, and CD54 significantly reduced cytotoxicity against CMV-infected cells. A combination of anti-CD11a, anti-CD11b, and anti-CD18 antibodies further inhibited cytotoxicity against CMV-infected cells. Cytotoxicity against CMV-infected cells treated with anti-CD54 antibody was also significantly inhibited. Binding of effector cells to target cells was not affected by treatment of NPBMC or CMV-infected cells with antiadhesion molecule antibodies. These results indicate that LFA-1 (CD11a/CD18), Mac-1 (CD11b/CD18), and ICAM-1 (CD54) adhesion molecules are involved in natural killer (NK) cell-induced DNA fragmentation in CMV-infected cells.

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Monoclonal antibodies against leucoagglutinin‐reactive human T lymphocyte surface components: Two antibodies which inhibit cell‐mediated cytotoxicity at a post‐binding stage

Vargas‐Cortes¹,

Hammarström²,

Hammarström³

et al. 1986

Eur J Immunol

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Two out of 20 monoclonal antibodies (IgM, kappa), mAb 3192 and mAb K3G, raised against leucoagglutinin-reactive components on human T cells, effectively blocked lymphocyte-mediated cytotoxicity in vitro. No antigenic polypeptide reactive with these antibodies has been identified thus far. However, they have previously been shown to react specifically with certain neutral glycolipids obtained from spleen. Both mAb inhibited the cytotoxicity of natural killer (NK) cells against K562 cells, antibody-dependent cellular cytotoxicity (ADCC) towards antibody-coated bovine erythrocytes and cytotoxic T lymphocyte activity against allogeneic target cells. In both NK and ADCC, preincubation of the lymphocytes with different antibody concentrations resulted in a dose-dependent reduction of cytotoxicity. In contrast, preincubation of the target cells had no effect indicating that the mAb inhibited cytotoxicity at the effector cell level. When studied at the single-cell level, the mAb did not alter the number of lymphocytes forming conjugates with K562 but significantly reduced the frequency of conjugates containing dead target cells. Addition of the mAb to preformed conjugates resulted in a dose-dependent reduction in the proportion of conjugates containing dead target cells. Furthermore, mAb 3192 did not reduce the number of lymphocytes forming rosettes with bovine erythrocytes, indicating that inhibition of ADCC was not due to blocking of the effector cell-target cell interaction mediated by the Fc receptor of the effector cells. Taken together, these results suggest that the mAb inhibited cytotoxicity by interfering with a post-binding step common for the different cytotoxicity systems.

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A monoclonal antibody (RH1-38) which inhibits multiple systems of cell-mediated cytotoxicity—II. Evidence that the epitope recognized is involved in a late step in the cytolytic mechanism

Cited by 10 publications

References 24 publications

Tumour necrosis factor-α induces an increase in susceptibility of human glioblastoma U87-MG cells to natural killer cell-mediated lysis

Tumour necrosis factor-α induces an increase in susceptibility of human glioblastoma U87-MG cells to natural killer cell-mediated lysis

Role of Adhesion Molecules in Natural Killer Cell-Induced DNA Fragmentation of Cytomegalovirus-Infected Fibroblasts

Monoclonal antibodies against leucoagglutinin‐reactive human T lymphocyte surface components: Two antibodies which inhibit cell‐mediated cytotoxicity at a post‐binding stage

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