| First Author | Seo SK | Year | 2003 |
| Journal | J Immunol | Volume | 171 |
| Issue | 2 | Pages | 576-83 |
| PubMed ID | 12847221 | Mgi Jnum | J:84287 |
| Mgi Id | MGI:2667275 | Doi | 10.4049/jimmunol.171.2.576 |
| Citation | Seo SK, et al. (2003) Blocking 4-1BB/4-1BB ligand interactions prevents herpetic stromal keratitis. J Immunol 171(2):576-83 |
| abstractText | Herpetic stromal keratitis (HSK) is a chronic inflammatory process in corneal stroma that results from recurrent HSV type 1 infection. We used the murine model of HSK to demonstrate the importance of the interaction between an inducible T cell costimulatory receptor, 4-1BB, and its ligand, 4-1BB ligand (4-1BBL), in the development of this disease. In BALB/c mice, HSK ordinarily induced by infection with the RE strain of herpes was prevented by blocking 4-1BB/4-1BBL interaction, either by deleting 4-1BB (in mutant 4-1BB(-/-) mice) or by introducing mAbs against 4-1BBL. The majority of T cells infiltrating the infected corneas were 4-1BB(+) activated effector cells that expressed cell surface markers CD44, CD25, and/or CD62L, as well as chemokine receptors CCR1, CCR2, and CCR5, and a limited number of TCR Vbeta chains (Vbeta8.1/8.2, Vbeta8.3, Vbeta10b, and Vbeta5.1/5.2, in order of abundance). Analysis of cell surface phenotypes showed that the failure to develop HSK in the 4-1BB(-/-) mice was associated with a reduced expression of CD62L at the time of T cell migration into the corneal stroma. |
