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Blocking 4-1BB/4-1BB Ligand Interactions Prevents Herpetic Stromal Keratitis¹

Su K. Seo^*, Hye Y. Park^*, Jae H. Choi^*, Won Y. Kim^*, Young H. Kim^*, Hyo W. Jung^*, Byungsuk Kwon^*, Hyeon W. Lee^* and Byoung S. Kwon^2,*,

^* Immunomodulation Research Center, University of Ulsan, Ulsan, Korea; and Louisiana State University Eye Center, Louisiana State University Health Sciences Center School of Medicine, New Orleans, LA 70112

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 V chains (V8.1/8.2, V8.3, V10b, and V5.1/5.2, 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.

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