Generation and characterization of a therapeutic human antibody to melanoma antigen TYRP1

Patel, Dhaval; Balderes, Paul; Lahiji, Armin; Melchior, Maxine; Ng, Stanley; Bassi, Rajiv; Wu, Yan; Griffith, Heather; Jimenez, Xenia; Ludwig, Dale L.; Hicklin, Daniel J.; Kang, Xiaoqiang

doi:10.3233/hab-2007-163-407

Cited by 30 publications

(36 citation statements)

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“…2). The affinity constant ( K d ) was found to be similar for both the antibody and the ADC and comparable to the reported K d values, 26–28 suggesting that the conformational change, if any, is local and does not impact the antigen-binding domains of the antibody.…”

Section: Resultssupporting

confidence: 79%

Development of a facile antibody–drug conjugate platform for increased stability and homogeneity

et al. 2017

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Section: Resultssupporting

confidence: 79%

Development of a facile antibody–drug conjugate platform for increased stability and homogeneity

et al. 2017

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“…A significant reduction in tumor load after CTA99 injection and an abolition of this effect after hFc␥RI blockade were also obtained in anti-Fc␥RIV mAb pretreated RAG-deficient hFc␥RI tg 5KO mice that cannot produce endogenous antibodies ( Figure 7D). Furthermore, injections of a fully human IgG1 mAb anti-TYRP-1 39 had a tendency to reduce tumor loads in hFc␥RI tg 5KO mice pretreated with anti-Fc␥RIV mAbs ( Figure 7E). Therefore, hFc␥RI mediates Ab-induced reduction of tumor load in transgenic mice after injection of humanized anti-TYRP-1 mAbs.…”

Section: Hfc␥ri Can Mediate Ab-induced Antitumor Immunotherapymentioning

confidence: 94%

The high-affinity human IgG receptor FcγRI (CD64) promotes IgG-mediated inflammation, anaphylaxis, and antitumor immunotherapy

Mancardi

Albanesi

Jönsson

et al. 2013

Blood

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129

112

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Key Points• Human Fc␥RI can trigger antibody-induced inflammatory arthritis, thrombocytopenia, airway inflammation, and systemic anaphylaxis.• Human Fc␥RI can trigger antibody-mediated immunotherapy of mouse metastatic melanoma.Receptors for the Fc portion of IgG (Fc␥Rs) are mandatory for the induction of various IgG-dependent models of autoimmunity, inflammation, anaphylaxis, and cancer immunotherapy. A few Fc␥Rs have the ability to bind monomeric IgG: high-affinity mouse mFc␥RI, mFc␥RIV, and human hFc␥RI. All others bind IgG only when aggregated in complexes or bound to cells or surfaces: low-affinity mouse mFc␥RIIB and mFc␥RIII and human hFc␥RIIA/B/C and hFc␥RIIIA/B. Although it has been proposed that high-affinity Fc␥Rs are occupied by circulating IgG, multiple roles for mFc␥RI and mFc␥RIV have been reported in vivo. However, the potential roles of hFc␥RI that is expressed on monocytes, macrophages, and neutrophils have not been reported. In the present study, we therefore investigated the role of hFc␥RI in antibody-mediated models of disease and therapy by generating hFc␥RI-transgenic mice deficient for multiple endogenous FcRs. hFc␥RI was sufficient to trigger autoimmune arthritis and thrombocytopenia, immune complex-induced airway inflammation, and active and passive systemic anaphylaxis. We found monocyte/macrophages to be responsible for thrombocytopenia, neutrophils to be responsible for systemic anaphylaxis, and both cell types to be responsible for arthritis induction.

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“…First, we studied a time course of neutrophil infiltration after administration of TA99. 24 and 48 h after the administration of TA99 at 40 mg/kg, [8] we collected mouse tumor tissues and performed the flow cytometry after staining with Alexa-Fluor-488-labeled anti-mouse Gr-1 to mark neutrophils. It is noted that the infiltration of neutrophils in tumor tissues was strongly dependent on TA99, and the percentage of neutrophils dramatically increased 48 h after the administration of TA99 (Figure 1A and S4A–S4D), suggesting that TA99 can facilitate the infiltration of neutrophils into tumor, which is consistent with the previous study.…”

Section: Antibody Increases the Accumulation Of Nps In Tumor Mediatedmentioning

confidence: 99%

“…[6] In a mouse model of B16 melanoma, it is found that monoclonal antibody TA99 specific for gp75 antigen can induce neutrophil recruitment in tumor sites as a mechanism of antibody-dependent cell-mediated cytotoxicity (ADCC) for cancer therapy, and neutrophils are a major component of ADCC effect rather than other immune effector cells. [7, 8] The interaction of neutrophils with tumor cells is mediated by the binding of antibody Fc portion to Fc receptors expressed on immune cells. [9] Targeting neutrophils in vivo using NPs could enhance the delivery of drugs in the tumor microenvironment.…”

mentioning

confidence: 99%

Nanoparticle Targeting of Neutrophils for Improved Cancer Immunotherapy

Zhao²,

et al. 2016

Adv Healthcare Materials

116

102

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Cancer immunotherapy using tumor specific monoclonal antibodies (mAbs) presents a novel approach for cancer treatment. A monoclonal antibody TA99 specific for gp75 antigen of melanoma, initiates neutrophil recruitment in tumor responsible for cancer therapy. Here we report a strategy for hijacking neutrophils in vivo using nanoparticles (NPs) to deliver therapeutics into tumor. In a mouse model of melanoma, we showed that systemically delivered albumin NPs increased in tumor when TA99 antibody was injected; and the nanoparticle tumor accumulation was mediated by neutrophils. After the administration of pyropheophorbide-a (Ppa) loaded albumin NPs and TA99, photodynamic therapy significantly suppressed the tumor growth and increased mouse survival compared with treatment with the NPs or TA99. The study reveals a new avenue to treat cancer by nanoparticle hitchhiking of immune systems to enhance delivery of therapeutics into tumor sites.

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Generation and characterization of a therapeutic human antibody to melanoma antigen TYRP1

Cited by 30 publications

References 0 publications

Development of a facile antibody–drug conjugate platform for increased stability and homogeneity

Development of a facile antibody–drug conjugate platform for increased stability and homogeneity

The high-affinity human IgG receptor FcγRI (CD64) promotes IgG-mediated inflammation, anaphylaxis, and antitumor immunotherapy

Nanoparticle Targeting of Neutrophils for Improved Cancer Immunotherapy

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