| First Author | Weighardt H | Year | 2015 |
| Journal | Eur J Immunol | Volume | 45 |
| Issue | 4 | Pages | 971-4 |
| PubMed ID | 25707546 | Mgi Jnum | J:229725 |
| Mgi Id | MGI:5753041 | Doi | 10.1002/eji.201545524 |
| Citation | Weighardt H, et al. (2015) Bcl-3 puts the brakes on contact hypersensitivity. Eur J Immunol 45(4):971-4 |
| abstractText | B-cell lymphoma (Bcl)-3 is a nonclassical member of the IkappaB protein family known to interact with transcriptionally inactive NF-kappaB1 and NF-kappaB2 homodimers to modulate gene expression. Besides its action as an oncoprotein, Bcl-3 has been shown to have both proinflammatory and anti-inflammatory functions depending on the cell-type affected. In this issue of the European Journal of Immunology, Tassi et al. [Eur. J. Immunol. 2015. 45: 1059-1068] report that Bcl-3 inhibits the production of the proinflammatory chemokines CXCL9 and CXCL10 in keratinocytes, thereby restricting the influx of CD8(+) effector T cells in a mouse model of allergic contact dermatitis. In addition, mice with a global deficiency of Bcl-3 show enhanced ear swelling responses in the late phase of contact hypersensitivity responses. Besides keratinocytes, other radioresistant cell types appear to also utilize Bcl-3 to dampen the inflammatory response. This Commentary will discuss the evidence supporting Bcl-3 as a critical player in limiting inflammation during the later stages of contact hypersensitivity. |
