Anti-human-TIGIT agonistic antibody ameliorates autoimmune diseases by inhibiting Tfh and Tph cells and enhancing Treg cells

T cells play important roles in autoimmune diseases, but it remains unclear how to optimally manipulate them. We focused on the T cell immunoreceptor with Ig and ITIM domains (TIGIT), a coinhibitory molecule that regulates and is expressed in T cells. In autoimmune diseases, the association between...

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Published inCommunications biology Vol. 6; no. 1; pp. 500 - 13
Main Authors Kojima, Marenori, Suzuki, Katsuya, Takeshita, Masaru, Ohyagi, Masaki, Iizuka, Mana, Yamane, Humitsugu, Koga, Keiko, Kouro, Taku, Kassai, Yoshiaki, Yoshihara, Tomoki, Adachi, Ryutaro, Hashikami, Kentarou, Ota, Yuichiro, Yoshimoto, Keiko, Kaneko, Yuko, Morita, Rimpei, Yoshimura, Akihiko, Takeuchi, Tsutomu
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 09.05.2023
Nature Publishing Group
Nature Portfolio
Subjects
13/31
64/60
692/4023/1670/1613
692/4023/1670/498
Agonistic behavior
Animals
Antibodies, Monoclonal - pharmacology
Autoimmune diseases
Autoimmune Diseases - drug therapy
Biology
Biomedical and Life Sciences
CD4 antigen
Cell activation
Immunoglobulins
Immunoreceptor tyrosine-based inhibition motif
Immunoregulation
Life Sciences
Lymphocytes
Lymphocytes T
Mice
Monoclonal antibodies
Receptors, Immunologic - genetics
Signal Transduction
T-Lymphocytes, Regulatory
Online AccessGet full text

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Abstract T cells play important roles in autoimmune diseases, but it remains unclear how to optimally manipulate them. We focused on the T cell immunoreceptor with Ig and ITIM domains (TIGIT), a coinhibitory molecule that regulates and is expressed in T cells. In autoimmune diseases, the association between TIGIT-expressing cells and pathogenesis and the function of human-TIGIT (hu-TIGIT) signalling modification have not been fully elucidated. Here we generated anti-hu-TIGIT agonistic monoclonal antibodies (mAbs) and generated hu- TIGIT knock-in mice to accurately evaluate the efficacy of mAb function. Our mAb suppressed the activation of CD4 + T cells, especially follicular helper T and peripheral helper T cells that highly expressed TIGIT, and enhanced the suppressive function of naïve regulatory T cells. These results indicate that our mAb has advantages in restoring the imbalance of T cells that are activated in autoimmune diseases and suggest potential clinical applications for anti-hu-TIGIT agonistic mAbs as therapeutic agents. A monoclonal human T cell immunoreceptor with Ig and ITIM domains (TIGIT) agonistic antibody in a TIGIT knock-in mouse model suppresses follicular and peripheral helper T cell activation and enhances suppression effects of naive regulatory T cells.
AbstractList T cells play important roles in autoimmune diseases, but it remains unclear how to optimally manipulate them. We focused on the T cell immunoreceptor with Ig and ITIM domains (TIGIT), a coinhibitory molecule that regulates and is expressed in T cells. In autoimmune diseases, the association between TIGIT-expressing cells and pathogenesis and the function of human-TIGIT (hu-TIGIT) signalling modification have not been fully elucidated. Here we generated anti-hu-TIGIT agonistic monoclonal antibodies (mAbs) and generated hu-TIGIT knock-in mice to accurately evaluate the efficacy of mAb function. Our mAb suppressed the activation of CD4+ T cells, especially follicular helper T and peripheral helper T cells that highly expressed TIGIT, and enhanced the suppressive function of naïve regulatory T cells. These results indicate that our mAb has advantages in restoring the imbalance of T cells that are activated in autoimmune diseases and suggest potential clinical applications for anti-hu-TIGIT agonistic mAbs as therapeutic agents.T cells play important roles in autoimmune diseases, but it remains unclear how to optimally manipulate them. We focused on the T cell immunoreceptor with Ig and ITIM domains (TIGIT), a coinhibitory molecule that regulates and is expressed in T cells. In autoimmune diseases, the association between TIGIT-expressing cells and pathogenesis and the function of human-TIGIT (hu-TIGIT) signalling modification have not been fully elucidated. Here we generated anti-hu-TIGIT agonistic monoclonal antibodies (mAbs) and generated hu-TIGIT knock-in mice to accurately evaluate the efficacy of mAb function. Our mAb suppressed the activation of CD4+ T cells, especially follicular helper T and peripheral helper T cells that highly expressed TIGIT, and enhanced the suppressive function of naïve regulatory T cells. These results indicate that our mAb has advantages in restoring the imbalance of T cells that are activated in autoimmune diseases and suggest potential clinical applications for anti-hu-TIGIT agonistic mAbs as therapeutic agents.
T cells play important roles in autoimmune diseases, but it remains unclear how to optimally manipulate them. We focused on the T cell immunoreceptor with Ig and ITIM domains (TIGIT), a coinhibitory molecule that regulates and is expressed in T cells. In autoimmune diseases, the association between TIGIT-expressing cells and pathogenesis and the function of human-TIGIT (hu-TIGIT) signalling modification have not been fully elucidated. Here we generated anti-hu-TIGIT agonistic monoclonal antibodies (mAbs) and generated hu- TIGIT knock-in mice to accurately evaluate the efficacy of mAb function. Our mAb suppressed the activation of CD4 + T cells, especially follicular helper T and peripheral helper T cells that highly expressed TIGIT, and enhanced the suppressive function of naïve regulatory T cells. These results indicate that our mAb has advantages in restoring the imbalance of T cells that are activated in autoimmune diseases and suggest potential clinical applications for anti-hu-TIGIT agonistic mAbs as therapeutic agents. A monoclonal human T cell immunoreceptor with Ig and ITIM domains (TIGIT) agonistic antibody in a TIGIT knock-in mouse model suppresses follicular and peripheral helper T cell activation and enhances suppression effects of naive regulatory T cells.
T cells play important roles in autoimmune diseases, but it remains unclear how to optimally manipulate them. We focused on the T cell immunoreceptor with Ig and ITIM domains (TIGIT), a coinhibitory molecule that regulates and is expressed in T cells. In autoimmune diseases, the association between TIGIT-expressing cells and pathogenesis and the function of human-TIGIT (hu-TIGIT) signalling modification have not been fully elucidated. Here we generated anti-hu-TIGIT agonistic monoclonal antibodies (mAbs) and generated hu- TIGIT knock-in mice to accurately evaluate the efficacy of mAb function. Our mAb suppressed the activation of CD4 + T cells, especially follicular helper T and peripheral helper T cells that highly expressed TIGIT, and enhanced the suppressive function of naïve regulatory T cells. These results indicate that our mAb has advantages in restoring the imbalance of T cells that are activated in autoimmune diseases and suggest potential clinical applications for anti-hu-TIGIT agonistic mAbs as therapeutic agents.
T cells play important roles in autoimmune diseases, but it remains unclear how to optimally manipulate them. We focused on the T cell immunoreceptor with Ig and ITIM domains (TIGIT), a coinhibitory molecule that regulates and is expressed in T cells. In autoimmune diseases, the association between TIGIT-expressing cells and pathogenesis and the function of human-TIGIT (hu-TIGIT) signalling modification have not been fully elucidated. Here we generated anti-hu-TIGIT agonistic monoclonal antibodies (mAbs) and generated hu-TIGIT knock-in mice to accurately evaluate the efficacy of mAb function. Our mAb suppressed the activation of CD4+ T cells, especially follicular helper T and peripheral helper T cells that highly expressed TIGIT, and enhanced the suppressive function of naïve regulatory T cells. These results indicate that our mAb has advantages in restoring the imbalance of T cells that are activated in autoimmune diseases and suggest potential clinical applications for anti-hu-TIGIT agonistic mAbs as therapeutic agents.A monoclonal human T cell immunoreceptor with Ig and ITIM domains (TIGIT) agonistic antibody in a TIGIT knock-in mouse model suppresses follicular and peripheral helper T cell activation and enhances suppression effects of naive regulatory T cells.
Abstract T cells play important roles in autoimmune diseases, but it remains unclear how to optimally manipulate them. We focused on the T cell immunoreceptor with Ig and ITIM domains (TIGIT), a coinhibitory molecule that regulates and is expressed in T cells. In autoimmune diseases, the association between TIGIT-expressing cells and pathogenesis and the function of human-TIGIT (hu-TIGIT) signalling modification have not been fully elucidated. Here we generated anti-hu-TIGIT agonistic monoclonal antibodies (mAbs) and generated hu-TIGIT knock-in mice to accurately evaluate the efficacy of mAb function. Our mAb suppressed the activation of CD4+ T cells, especially follicular helper T and peripheral helper T cells that highly expressed TIGIT, and enhanced the suppressive function of naïve regulatory T cells. These results indicate that our mAb has advantages in restoring the imbalance of T cells that are activated in autoimmune diseases and suggest potential clinical applications for anti-hu-TIGIT agonistic mAbs as therapeutic agents.
T cells play important roles in autoimmune diseases, but it remains unclear how to optimally manipulate them. We focused on the T cell immunoreceptor with Ig and ITIM domains (TIGIT), a coinhibitory molecule that regulates and is expressed in T cells. In autoimmune diseases, the association between TIGIT-expressing cells and pathogenesis and the function of human-TIGIT (hu-TIGIT) signalling modification have not been fully elucidated. Here we generated anti-hu-TIGIT agonistic monoclonal antibodies (mAbs) and generated hu-TIGIT knock-in mice to accurately evaluate the efficacy of mAb function. Our mAb suppressed the activation of CD4 T cells, especially follicular helper T and peripheral helper T cells that highly expressed TIGIT, and enhanced the suppressive function of naïve regulatory T cells. These results indicate that our mAb has advantages in restoring the imbalance of T cells that are activated in autoimmune diseases and suggest potential clinical applications for anti-hu-TIGIT agonistic mAbs as therapeutic agents.
ArticleNumber 500
Author Kouro, Taku
Ohyagi, Masaki
Takeuchi, Tsutomu
Kojima, Marenori
Yoshimoto, Keiko
Yoshimura, Akihiko
Suzuki, Katsuya
Yamane, Humitsugu
Kaneko, Yuko
Koga, Keiko
Ota, Yuichiro
Hashikami, Kentarou
Kassai, Yoshiaki
Yoshihara, Tomoki
Adachi, Ryutaro
Takeshita, Masaru
Iizuka, Mana
Morita, Rimpei
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Snippet T cells play important roles in autoimmune diseases, but it remains unclear how to optimally manipulate them. We focused on the T cell immunoreceptor with Ig...
Abstract T cells play important roles in autoimmune diseases, but it remains unclear how to optimally manipulate them. We focused on the T cell immunoreceptor...
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SubjectTerms 13/31
64/60
692/4023/1670/1613
692/4023/1670/498
Agonistic behavior
Animals
Antibodies, Monoclonal - pharmacology
Autoimmune diseases
Autoimmune Diseases - drug therapy
Biology
Biomedical and Life Sciences
CD4 antigen
Cell activation
Immunoglobulins
Immunoreceptor tyrosine-based inhibition motif
Immunoregulation
Life Sciences
Lymphocytes
Lymphocytes T
Mice
Monoclonal antibodies
Receptors, Immunologic - genetics
Signal Transduction
T-Lymphocytes, Regulatory
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Title Anti-human-TIGIT agonistic antibody ameliorates autoimmune diseases by inhibiting Tfh and Tph cells and enhancing Treg cells
URI https://link.springer.com/article/10.1038/s42003-023-04874-3
https://www.ncbi.nlm.nih.gov/pubmed/37161050
https://www.proquest.com/docview/2811429320
https://www.proquest.com/docview/2811939146
https://pubmed.ncbi.nlm.nih.gov/PMC10170076
https://doaj.org/article/f0cee47f61f749aca6573a414bdab36e
Volume 6
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