Pulmonary metastases neutralization and tumor rejection byin vivo administration of β glucan and bispecific antibody

Penna, Christophe; Dean, Philip A. W.; Nelson, Heidi D

doi:10.1002/(sici)1097-0215(19960126)65:3<377::aid-ijc17>3.0.co;2-7

Cited by 9 publications

(1 citation statement)

References 20 publications

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“…Bispecific antibodies (BsAb) and superantigens have both been used individually and in combination in the treatment of solid malignant tumor models resembling metastatic disease because these models are easily targeted with immunotherapy [1][2][3]. The effector cells responsible for the cytolytic destruction of the tumor are considered to be the primary cells involved in protective immunity [4 -7].…”

Section: Introductionmentioning

confidence: 99%

Depletion of activated Vβ8+ T cells disrupts bispecific antibody directed antitumor immunity1

McConnell

McLemore

Talac

et al. 2004

Journal of Surgical Research

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Section: Introductionmentioning

confidence: 99%

Depletion of activated Vβ8+ T cells disrupts bispecific antibody directed antitumor immunity1

McConnell

McLemore

Talac

et al. 2004

Journal of Surgical Research

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Tumor-infiltrating lymphocytes can be activatedin situ by usingin vivo activants plus F(ab′)2 bispecific antibodies

1996

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In vitro-activated T lymphocytes can be retargeted with anti-CD3 X anti-tumor bispecific antibodies (BsAb) t o kill tumor cells in vitro and in vivo. The purpose of the present study was to examine the systemic and intra-tumor effects of in vivo T-cell activation with BsAb, staphylococcal enterotoxin B (SEB), and P-glucan in combination with BsAb as a retargeting agent. CL-62 melanoma cells were injected subcutaneously into C3H/ HeN mice. Mice were subsequently treated with BsAb alone or with SEB or P-glucan plus BsAb. Fresh splenocytes, lymph-node cells and tumor-infiltrating lymphocytes (TlL) were tested for their proliferative response using incorporation of 3H-thymidine, and for their ability to lyse CL-62 cells in the presence or absence of BsAb in 4-hr S'Chromium release assays. Toxicity of treatments was assessed in a D-galactosamine model. BsAb, alone or combined with P-glucan, had essentially no effect on systemic T-cell cytotoxicity, and essentially no effect on systemic proliferation, unless exogenous IL-2 was provided. A t the tumor site, BsAb alone, BsAb plus P-glucan, and SEB plus BsAb all significantly increased BsAb-mediated TIL cytotoxicity. In contrast to the TIL-limited effects of BsAb and of BsAb plus p-glucan, SEB plus BsAb markedly increased both systemic and intra-tumor T-lymphocyte activation. Toxicity correlated with measures of systemic activation, with limited effects from BsAb alone and from P-glucan plus BsAb, and with marked lethality from SEB plus BsAb. Overall, these results suggest moderate intra-tumor activation of TIL, but no measurable systemic activation after in vivo treatment with BsAb or p-glucan plus BsAb. SEB plus BsAb results in complete T-cell activation in both systemic and intra-tumor compartments, but at the expense of increased systemic toxicity. In conclusion, TIL can be activated in situ with different combinations of in vivo activants. In vivo-activated TIL can be retargeted with bispecific antibodies to lyse tumor cells, and may be an alternative to ex vivo T-cell activation and adoptive transfer therapy.o 1996 Wiley-Liss, Inc.

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Bispecific antibody and its clinical applications in cancer

Yang

Zhu

2001

Chin.Sci.Bull.

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Pulmonary metastases neutralization and tumor rejection byin vivo administration of β glucan and bispecific antibody

Abstract: o 1996 Wiley-Liss, Inc.

Cited by 9 publications

References 20 publications

Depletion of activated Vβ8+ T cells disrupts bispecific antibody directed antitumor immunity1

Depletion of activated Vβ8+ T cells disrupts bispecific antibody directed antitumor immunity1

Tumor-infiltrating lymphocytes can be activatedin situ by usingin vivo activants plus F(ab′)2 bispecific antibodies

Bispecific antibody and its clinical applications in cancer

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