Herpes simplex virus (HSV)-1-infected BALB/c mice with necrotizing HSK were treated with AMT. Early preclinical events include inflammatory cell, mainly neutrophils, infiltration of the stroma, and neovascularization. We investigated the possibility that there might be differential Vβ preferential usage in HSK resistant and susceptible BALB/c congenic mice that differ only in a small region associated with the Igh-1 gene locus. Results: On day 10 postinfection (pi), the RAPA group showed only a significantly lower angiogenic development than the CG. In the stroma, VEGF was produced by inflammatory cells; these initially were predominantly polymorphonuclear leukocytes (PMN), but at later time points both PMN and macrophage-like cells were VEGF producers. Treatment of mice with a depleting anti-lymphotoxin-α mAb during the clinical phase of the disease significantly attenuated stromal keratitis lesions. expression before and during clinical disease with a decline thereafter.
IL-4 levels peaked and declined before day 14, while IL-10 peaked on days 7 or 14 and paralleled IFN? at lower levels. Small amounts of IL-12 p40 mRNA were detected late in the disease course. Since genuine autoimmune HSK without HSV growth can hardly be the case in clinical practice, some part of these new theories remains controversial. 1 and 2). These data suggest that disease resolution in corneas with recurrent HSK may depend upon the balance between destructive and protective cytokines at individual sites of viral recurrence.