Murinization and H Chain Isotype Matching of the Anti-GITR Antibody DTA-1 Reduces Immunogenicity-Mediated Anaphylaxis in C57BL/6 Mice
Recent advances in immuno-oncology have shown that the immune system can be activated to induce long-term, durable antitumor responses. For immuno-oncology drug development, immune activation is often explored using rat Abs in immunocompetent mouse models. Although these models can be used to show e...
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Published in | The Journal of immunology (1950) Vol. 198; no. 11; pp. 4502 - 4512 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
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American Association of Immunologists
01.06.2017
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Abstract | Recent advances in immuno-oncology have shown that the immune system can be activated to induce long-term, durable antitumor responses. For immuno-oncology drug development, immune activation is often explored using rat Abs in immunocompetent mouse models. Although these models can be used to show efficacy, antidrug immune responses to experimental protein-based therapeutics can arise. Immunogenicity of surrogate Abs may therefore represent an important obstacle to the evaluation of the antitumor efficacy of immunomodulator Abs in syngeneic models. A recent publication has shown that anti-glucocorticoid-induced TNFR family-related protein agonistic Ab DTA-1 (rat or murinized IgG2a) can induce the development of anaphylaxis in C57BL/6 mice upon repeated i.p. dosing because of an anti-idiotypic anti-drug Ab immune response. This study was undertaken to address the impact of the immunogenicity derived from the Fc and variable domains. To this end, chimerized (rat V domains/mouse constant regions) and murinized (95% mouse sequence) DTA-1-based surrogate Abs with a murine IgG2c H chain isotype were created. Chimerization and murinization of DTA-1 did not affect receptor binding and glucocorticoid-induced TNFR family-related protein-induced T cell agonistic properties. Similar in vivo antitumor efficacy and intratumoral CD8
/regulatory T cells were also observed. Finally, treatment of C57BL/6 mice with the chimerized and murinized DTA-1 Abs on a C57BL/6-matched IgG2c isotype resulted in reduced development and severity of anaphylaxis as measured by decline of body temperature, behavioral effects, serum IL-4, IgE, and anti-drug Ab levels. These results suggest that careful murinization and selection of a strain-matched H chain isotype are critical to generate ideal surrogate Abs for testing immuno-oncology mechanisms in vivo. |
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AbstractList | Recent advances in immuno-oncology have shown that the immune system can be activated to induce long-term, durable antitumor responses. For immuno-oncology drug development, immune activation is often explored using rat Abs in immunocompetent mouse models. Although these models can be used to show efficacy, antidrug immune responses to experimental protein-based therapeutics can arise. Immunogenicity of surrogate Abs may therefore represent an important obstacle to the evaluation of the antitumor efficacy of immunomodulator Abs in syngeneic models. A recent publication has shown that anti-glucocorticoid–induced TNFR family–related protein agonistic Ab DTA-1 (rat or murinized IgG2a) can induce the development of anaphylaxis in C57BL/6 mice upon repeated i.p. dosing because of an anti-idiotypic anti-drug Ab immune response. This study was undertaken to address the impact of the immunogenicity derived from the Fc and variable domains. To this end, chimerized (rat V domains/mouse constant regions) and murinized (95% mouse sequence) DTA-1–based surrogate Abs with a murine IgG2c H chain isotype were created. Chimerization and murinization of DTA-1 did not affect receptor binding and glucocorticoid-induced TNFR family–related protein–induced T cell agonistic properties. Similar in vivo antitumor efficacy and intratumoral CD8+/regulatory T cells were also observed. Finally, treatment of C57BL/6 mice with the chimerized and murinized DTA-1 Abs on a C57BL/6-matched IgG2c isotype resulted in reduced development and severity of anaphylaxis as measured by decline of body temperature, behavioral effects, serum IL-4, IgE, and anti-drug Ab levels. These results suggest that careful murinization and selection of a strain-matched H chain isotype are critical to generate ideal surrogate Abs for testing immuno-oncology mechanisms in vivo. Recent advances in immuno-oncology have shown that the immune system can be activated to induce long-term, durable antitumor responses. For immuno-oncology drug development, immune activation is often explored using rat Abs in immunocompetent mouse models. Although these models can be used to show efficacy, antidrug immune responses to experimental protein-based therapeutics can arise. Immunogenicity of surrogate Abs may therefore represent an important obstacle to the evaluation of the antitumor efficacy of immunomodulator Abs in syngeneic models. A recent publication has shown that anti-glucocorticoid-induced TNFR family-related protein agonistic Ab DTA-1 (rat or murinized IgG2a) can induce the development of anaphylaxis in C57BL/6 mice upon repeated i.p. dosing because of an anti-idiotypic anti-drug Ab immune response. This study was undertaken to address the impact of the immunogenicity derived from the Fc and variable domains. To this end, chimerized (rat V domains/mouse constant regions) and murinized (95% mouse sequence) DTA-1-based surrogate Abs with a murine IgG2c H chain isotype were created. Chimerization and murinization of DTA-1 did not affect receptor binding and glucocorticoid-induced TNFR family-related protein-induced T cell agonistic properties. Similar in vivo antitumor efficacy and intratumoral CD8 /regulatory T cells were also observed. Finally, treatment of C57BL/6 mice with the chimerized and murinized DTA-1 Abs on a C57BL/6-matched IgG2c isotype resulted in reduced development and severity of anaphylaxis as measured by decline of body temperature, behavioral effects, serum IL-4, IgE, and anti-drug Ab levels. These results suggest that careful murinization and selection of a strain-matched H chain isotype are critical to generate ideal surrogate Abs for testing immuno-oncology mechanisms in vivo. |
Author | Samayoa, Josue A Fox, Melvin I Tran, Ninian N Harding, Fiona A Hollenbaugh, Diane Chan, Sarah W Alvarez, Hamsell M Stickler, Marcia M Akamatsu, Yoshiko Belmar, Nicole A |
Author_xml | – sequence: 1 givenname: Nicole A surname: Belmar fullname: Belmar, Nicole A organization: Oncology Biologics Department, AbbVie Biotherapeutics Inc., Redwood City, CA 94063 – sequence: 2 givenname: Sarah W surname: Chan fullname: Chan, Sarah W organization: Oncology Biologics Department, AbbVie Biotherapeutics Inc., Redwood City, CA 94063 – sequence: 3 givenname: Melvin I surname: Fox fullname: Fox, Melvin I organization: Oncology Biologics Department, AbbVie Biotherapeutics Inc., Redwood City, CA 94063 – sequence: 4 givenname: Josue A surname: Samayoa fullname: Samayoa, Josue A organization: Oncology Biologics Department, AbbVie Biotherapeutics Inc., Redwood City, CA 94063 – sequence: 5 givenname: Marcia M surname: Stickler fullname: Stickler, Marcia M organization: Oncology Biologics Department, AbbVie Biotherapeutics Inc., Redwood City, CA 94063 – sequence: 6 givenname: Ninian N surname: Tran fullname: Tran, Ninian N organization: Oncology Biologics Department, AbbVie Biotherapeutics Inc., Redwood City, CA 94063 – sequence: 7 givenname: Yoshiko surname: Akamatsu fullname: Akamatsu, Yoshiko organization: Oncology Biologics Department, AbbVie Biotherapeutics Inc., Redwood City, CA 94063 – sequence: 8 givenname: Diane surname: Hollenbaugh fullname: Hollenbaugh, Diane organization: Oncology Biologics Department, AbbVie Biotherapeutics Inc., Redwood City, CA 94063 – sequence: 9 givenname: Fiona A orcidid: 0000-0003-3817-1203 surname: Harding fullname: Harding, Fiona A organization: Oncology Biologics Department, AbbVie Biotherapeutics Inc., Redwood City, CA 94063 – sequence: 10 givenname: Hamsell M surname: Alvarez fullname: Alvarez, Hamsell M email: hamsell.alvarezjares@abbvie.com organization: Oncology Biologics Department, AbbVie Biotherapeutics Inc., Redwood City, CA 94063 hamsell.alvarezjares@abbvie.com |
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CitedBy_id | crossref_primary_10_1016_j_ymthe_2020_02_007 crossref_primary_10_1038_s43018_022_00334_9 crossref_primary_10_1186_s40425_019_0671_4 |
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SubjectTerms | Anaphylaxis Anaphylaxis - immunology Animal models Animals Antitumor activity Body temperature Cancer immunotherapy CD8 antigen CD8-Positive T-Lymphocytes - immunology Cell Line, Tumor Drug development Glucocorticoid-Induced TNFR-Related Protein - immunology Glucocorticoids Immune response Immunogenicity Immunoglobulin E Immunoglobulin G Immunoglobulin Isotypes - immunology Immunoregulation Interleukin 4 Interleukin-4 - immunology Lymphocytes Lymphocytes T Mice Mice, Inbred C57BL Oncology Proteins Rats Receptors, IgG - immunology Strain T-Lymphocytes, Regulatory - immunology Tumor necrosis factor receptors |
Title | Murinization and H Chain Isotype Matching of the Anti-GITR Antibody DTA-1 Reduces Immunogenicity-Mediated Anaphylaxis in C57BL/6 Mice |
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