| First Author | Sommer C | Year | 2024 |
| Journal | Eur J Immunol | Volume | 54 |
| Issue | 4 | Pages | e2350580 |
| PubMed ID | 38430129 | Mgi Jnum | J:357773 |
| Mgi Id | MGI:7619160 | Doi | 10.1002/eji.202350580 |
| Citation | Sommer C, et al. (2024) Interleukin-2-induced skin inflammation. Eur J Immunol :e2350580 |
| abstractText | Recombinant human IL-2 has been used to treat inflammatory diseases and cancer; however, side effects like skin rashes limit the use of this therapeutic. To identify key molecules and cells inducing this side effect, we characterized IL-2-induced cutaneous immune reactions and investigated the relevance of CD25 (IL-2 receptor alpha) in the process. We injected IL-2 intradermally into WT mice and observed increases in immune cell subsets in the skin with preferential increases in frequencies of IL-4- and IL-13-producing group 2 innate lymphoid cells and IL-17-producing dermal gammadelta T cells. This overall led to a shift toward type 2/type 17 immune responses. In addition, using a novel topical genetic deletion approach, we reduced CD25 on skin, specifically on all cutaneous cells, and found that IL-2-dependent effects were reduced, hinting that CD25 - at least partly - induces this skin inflammation. Reduction of CD25 specifically on skin Tregs further augmented IL-2-induced immune cell infiltration, hinting that CD25 on skin Tregs is crucial to restrain IL-2-induced inflammation. Overall, our data support that innate lymphoid immune cells are key cells inducing side effects during IL-2 therapy and underline the significance of CD25 in this process. |
