皮膚に残る「再燃の火種」を発見―アレルギー性皮膚炎の再燃予防へ―

2026-10-13 京都大学

作成：朝比奈良太｜生成AI：OpenAI ChatGPT（GPT-5.6 Sol）

＜関連情報＞

• https://www.kyoto-u.ac.jp/ja/research-news/2026-10-13
• https://www.cell.com/immunity/abstract/S1074-7613(26)00385-7

⽪膚常在性CXCR6陽性記憶CD4陽性T細胞と樹状細胞は、アレルギー性⽪膚炎の再燃を駆動する真⽪⾎管周囲の免疫拠点を形成する Skin-resident CXCR6+ memory CD4+ T cells and dendritic cells form dermal perivascular hubs that drive relapse in allergic dermatitis

Ryota Asahina ∙ Fuuka Minami ∙ Satoshi Nakamizo ∙ … ∙ Akihiko Kitoh ∙ Gyohei Egawa ∙ Kenji Kabashima
Immunity  Published:October 12, 2026
DOI:https://doi.org/10.1016/j.immuni.2026.09.010

Highlights

• Pathogenic CXCR6⁺ CD4⁺ T_RM subset drives relapse in allergic skin diseases
• CXCR6⁺ CD4⁺ T_RM cells are sustained by CXCL16-mediated clustering with CD301b⁺ cDC2s
• CXCR6⁺ T_RM-cDC2 clusters persist in human AD lesions after anti-IL-13 therapy
• CXCL16-CXCR6 blockade disrupts relapse-driving T_RM niches in allergic dermatitis

Summary

CD4⁺ tissue-resident memory T (T_RM) cells are crucial for relapse in allergic skin conditions. However, the mechanisms underlying their maintenance and pathogenic potential remain poorly defined. Here, across multiple models of allergic dermatitis, we identified a C-X-C chemokine receptor 6 (CXCR6⁺) subpopulation within CD4⁺ T_RM cells as a distinct pathogenic subset that rapidly induces relapse. This subset is supported by C-X-C chemokine ligand 16 (CXCL16)-dependent interactions with CD301b⁺ conventional type 2 dendritic cells (cDC2s) for in situ maintenance. Functional blockade of the CXCL16-CXCR6 signaling pathway impaired proliferation and maintenance of CXCR6⁺ CD4⁺ T_RM cells. In human atopic dermatitis (AD), CXCR6⁺ CD4⁺ T_RM cells co-localized with CD301⁺ cDC2s in perivascular clusters even after successful anti-IL-13 therapy. These findings point to CXCR6⁺ CD4⁺ T_RM cells as a pathogenic reservoir sustaining chronic and recurrent inflammation and suggest the CXCL16-CXCR6 axis as a therapeutic target to prevent relapse in allergic skin diseases.