| First Author | Liu J | Year | 2014 |
| Journal | J Invest Dermatol | Volume | 134 |
| Issue | 7 | Pages | 1903-1911 |
| PubMed ID | 24487305 | Mgi Jnum | J:210539 |
| Mgi Id | MGI:5571421 | Doi | 10.1038/jid.2014.61 |
| Citation | Liu J, et al. (2014) IL-9 Regulates Allergen-Specific Th1 Responses in Allergic Contact Dermatitis. J Invest Dermatol 134(7):1903-11 |
| abstractText | The cytokine IL-9, derived primarily from T-helper 9 (Th9) lymphocytes, promotes expansion of the Th2 subset and is implicated in the mechanisms of allergic asthma. We hypothesize that IL-9 also has a role in human allergic contact dermatitis (ACD). To investigate this hypothesis, skin biopsy specimens of positive patch-test sites from non-atopic patients were assayed using quantitative PCR and immunohistochemistry. The cytokines IFN-gamma, IL-4, IL-17A, IL-9, and PU.1, a Th9 associated transcription factor, were elevated when compared with paired normal skin. Immunohistochemistry on ACD skin biopsies identified PU.1(+)CD3(+) and PU.1(+)CD4(+) cells, consistent with Th9 lymphocytes, in the inflammatory infiltrate. Peripheral blood mononuclear cells from nickel-allergic patients, but not nonallergic controls, show significant IL-9 production in response to nickel. Blocking studies with mAbs to HLA-DR (but not HLA-A, -B, -C) or chloroquine significantly reduced this nickel-specific IL-9 production. In addition, blockade of IL-9 or IL-4 enhanced allergen-specific IFN-gamma production. A contact hypersensitivity model using IL-9(-/-) mice shows enhanced Th1 lymphocyte immune responses, when compared with wild-type mice, consistent with our human in vitro data. This study demonstrates that IL-9, through its direct effects on Th1 and ability to promote IL-4 secretion, has a regulatory role for Th1 lymphocytes in ACD. |
