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DOI 10.1016/j.bbrc.2021.03.025

Медицинская библиотека · Biochemical and biophysical research communications · 2021

New inducible mast cell-deficient mouse model (Mcpt5/Cma1DTR).

Sasaki Hayato, Imanishi Madoka, Fujikura Daisuke, Sugiyama Makoto, Tanimoto Kyosuke, Mochiji Yohei, Takahashi Yuki, Hiura Koki, Watanabe Masaki, Kashimoto Takashige, Nakano Kenta, Okamura Tadashi, Sasaki Nobuya

СтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

Mast cell-deficient mice are helpful for understanding the roles of mast cells in vivo. To date, a dozen mouse models for mast cell deficiency have been reported. However, mice with a specific depletion of all populations of mast cells have not been reported. We generated knock-in mice, termed Mcpt5/Cma1DTR mice, expressing human diphtheria toxin A (DT) receptor under the endogenous promoter of Mcpt5 (also known as Cma1), which encodes mouse mast cell protease-5. Flow cytometry and histological analysis showed that intraperitoneal injection of DT induced almost complete depletion of mast cells in heterozygote Mcpt5/Cma1DTR/+ mice. The deletion rates of mast cells in peritoneal cavity, mesentery, abdominal skin, ear skin, and glandular stomach were 99.9%, 100%, 98.7%, 97.7%, and 100%, respectively. Passive cutaneous anaphylaxis reaction also revealed mast cell deficiency in ear skin after DT treatment. Other than mast cells, a small percentage of marginal zone B cells in Mcpt5/Cma1DTR/+ mice were killed by DT treatment. In conclusion, the Mcpt5/Cma1DTR/+ mouse model is valuable for achieving conditional depletion of all populations of mast cells without inducing a marked reduction in other cells.

Для цитирования: Sasaki Hayato, Imanishi Madoka, Fujikura Daisuke, Sugiyama Makoto, Tanimoto Kyosuke, Mochiji Yohei, Takahashi Yuki, Hiura Koki, Watanabe Masaki, Kashimoto Takashige, Nakano Kenta, Okamura Tadashi, Sasaki Nobuya. New inducible mast cell-deficient mouse model (Mcpt5/Cma1DTR).. Biochemical and biophysical research communications. 2021. DOI: 10.1016/j.bbrc.2021.03.025.

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