| First Author | Park HJ | Year | 2023 |
| Journal | Int J Mol Sci | Volume | 24 |
| Issue | 12 | PubMed ID | 37373104 |
| Mgi Jnum | J:337439 | Mgi Id | MGI:7495102 |
| Doi | 10.3390/ijms24129956 | Citation | Park HJ, et al. (2023) IL-7 Deficiency Exacerbates Atopic Dermatitis in NC/Nga Mice. Int J Mol Sci 24(12) |
| abstractText | Interleukin-7 (IL-7) plays a vital role in the homeostasis of CD4(+) and CD8(+) T cells. Although IL-7 has been implicated in T helper (Th)1- and Th17-mediated autoinflammatory diseases, its role in Th2-type allergic disorders, such as atopic dermatitis (AD), remains unclear. Thus, to elucidate the effects of IL-7 deficiency on AD development, we generated IL-7-deficient AD-prone mice by backcrossing IL-7 knockout (KO) B6 mice onto the NC/Nga (NC) mouse strain, a model for human AD. As expected, IL-7 KO NC mice displayed defective development of conventional CD4(+) and CD8(+) T cells compared with wild type (WT) NC mice. However, IL-7 KO NC mice presented with enhanced AD clinical scores, IgE hyperproduction, and increased epidermal thickness compared with WT NC mice. Moreover, IL-7 deficiency decreased Th1, Th17, and IFN-gamma-producing CD8(+) T cells but increased Th2 cells in the spleen of NC mice, indicating that a reduced Th1/Th2 ratio correlates with severity of AD pathogenesis. Furthermore, significantly more basophils and mast cells infiltrated the skin lesions of IL-7 KO NC mice. Taken together, our findings suggest that IL-7 could be a useful therapeutic target for treating Th2-mediated skin inflammations, such as AD. |
