2026-07-01 広島大学
図1：2種類のクローンマウス系統(Df#1、Df#2)の皮膚にダニ抗原(Der-f)を塗布し、発症する病態を調べました。両系統とも、炎症細胞浸潤を伴うアトピー性皮膚炎様病態を示しました。
＜関連情報＞
- https://www.hiroshima-u.ac.jp/news/98592
- https://www.sciencedirect.com/science/article/pii/S1323893026000778
アレルゲン特異的T細胞受容体クローン型の違いが、アトピー性皮膚炎のクローンマウスモデルにおいて異なる免疫プログラムを引き起こす Distinct allergen-specific T cell receptor clonotypes drive divergent immune programs in a cloned mouse model of atopic dermatitis
Uyanga Enkhbaatar, Kento Miura, Norimasa Yamasaki, Sawako Ogata, Ryoken Yamanaka, Fatemeh Beygom Mirkatouli, Anarkhuu Bold-Erdene, Tomofumi Numata, Tomoharu Yasuda, Kazumitsu Sugiura, Megumi Sasatani, Takashi Yamamoto, Kimiko Inoue, Atsuo Ogura, Osamu Kaminuma
Allergology International Available online 24 June 2026
DOI:https://doi.org/10.1016/j.alit.2026.06.001
Dear Editor,
Atopic dermatitis (AD) is a chronic inflammatory disease characterized by intense pruritus, epidermal barrier dysfunction, and type 2-dominant immune responses.1,2 Allergen-specific CD4+ T cells orchestrate cutaneous inflammation by producing cytokines such as IL-4, IL-13, and IL-17, promoting pruritus, epidermal hyperplasia, and IgE production.3 These responses are governed by allergen recognition via the T-cell receptor (TCR) αβ chains on CD4+ T cells.4 The TCRαβ repertoire diversity is thought to shape the quality and magnitude of cutaneous immune responses, affecting effector function, cytokine polarization, and disease severity.5, 6, 7 However, whether distinct TCR clonotypes directly program discrete immune outputs during allergic skin inflammation remains unknown.
