The IL‐13–OVOL 1–FLG axis in atopic dermatitis
K Furue, T Ito, G Tsuji, D Ulzii, YH Vu… - …, 2019 - Wiley Online Library
K Furue, T Ito, G Tsuji, D Ulzii, YH Vu, M Kido‐Nakahara, T Nakahara, M Furue
Immunology, 2019•Wiley Online LibraryDespite sharing interleukin‐4 receptor α (IL‐4Rα) in their signaling cascades, IL‐4 and IL‐
13 have different functions in atopic inflammation. IL‐13 preferentially participates in the
peripheral tissues because tissue‐resident group 2 innate lymphoid cells produce IL‐13 but
not IL‐4. In contrast, lymph node T follicular helper cells express IL‐4 but not IL‐13 to
regulate B‐cell immunity. The dominant microenvironment of IL‐13 is evident in the lesional
skin of atopic dermatitis (AD). The IL‐13‐rich local milieu causes barrier dysfunction by …
13 have different functions in atopic inflammation. IL‐13 preferentially participates in the
peripheral tissues because tissue‐resident group 2 innate lymphoid cells produce IL‐13 but
not IL‐4. In contrast, lymph node T follicular helper cells express IL‐4 but not IL‐13 to
regulate B‐cell immunity. The dominant microenvironment of IL‐13 is evident in the lesional
skin of atopic dermatitis (AD). The IL‐13‐rich local milieu causes barrier dysfunction by …
Summary
Despite sharing interleukin‐4 receptor α (IL‐4Rα) in their signaling cascades, IL‐4 and IL‐13 have different functions in atopic inflammation. IL‐13 preferentially participates in the peripheral tissues because tissue‐resident group 2 innate lymphoid cells produce IL‐13 but not IL‐4. In contrast, lymph node T follicular helper cells express IL‐4 but not IL‐13 to regulate B‐cell immunity. The dominant microenvironment of IL‐13 is evident in the lesional skin of atopic dermatitis (AD). The IL‐13‐rich local milieu causes barrier dysfunction by down‐regulating the OVOL1–filaggrin (FLG) axis and up‐regulating the periostin–IL‐24 axis. Genome‐wide association studies also point to the crucial involvement of the IL‐13, OVOL1 and FLG genes in the pathogenesis of AD. Biologics targeting IL‐13, such as the anti‐IL‐4Rα antibody dupilumab and the anti‐IL‐13 antibody tralokinumab, successfully improve AD lesions and further highlight the importance of IL‐13 in the pathogenesis of AD.
Wiley Online Library