Ghiasi H, Cai S, Slanina S, Nesburn A B, Wechsler S L
Cedars-Sinai Medical Center Research Institute, Los Angeles, California, USA.
Invest Ophthalmol Vis Sci. 1997 May;38(6):1213-21.
To determine whether the exacerbation of herpes simplex virus type-1 (HSV-1) induced corneal scarring that the authors reported previously in HSV-1 glycoprotein K (gK) vaccinated BALB/c mice challenged with HSV-1 strain McKrae was a general phenomenon independent of virus and mouse strains. To determine the gK-induced immune response leading to exacerbation of HSV-1-induced corneal scarring.
BALB/c or C57BL/6 mice were vaccinated with gK, ocularly challenged with HSV-1 strain KOS or McKrae, and the relative amount of corneal scarring determined 28 days after challenge. The T cells, total serum, or purified immunoglobulin G (IgG) isolated from gK-vaccinated mice was transferred individually to naive mice, and the affects on corneal scarring after HSV-1 challenge were determined.
The KOS challenge of gK-vaccinated BALB/c mice resulted in significant corneal scarring (P = 0.0003), despite the fact that KOS normally produces no corneal scarring. McKrae challenge of gK-vaccinated C57BL/6 mice resulted in significant corneal scarring (P < 0.0001), despite the fact that C57BL/6 mice are normally refractory to HSV-1-induced corneal scarring. Passive transfer of total anti-gK mouse sera or purified anti-gK mouse IgG, but not adoptive transfer of total anti-gK T-cells to naive mice, resulted in exacerbation of corneal scarring after HSV-1 challenge (P < 0.0001). Mice defective for T-cell-dependent antibody production were not susceptible to exacerbation of HSV-1-induced corneal scarring by gK vaccination (P < 0.0001).
The ability of gK vaccination to exacerbate HSV-1-induced corneal scarring was not mouse strain or HSV-1 strain specific. The gK-induced exacerbation of corneal scarring was related to anti-gK IgG. How anti-gK IgG exacerbated HSV-1 induced corneal scarring remains to be determined.
确定作者之前报道的在接种单纯疱疹病毒1型（HSV-1）糖蛋白K（gK）的BALB/c小鼠中，用HSV-1 McKrae株攻击后出现的HSV-1诱导的角膜瘢痕加重是否是一种与病毒和小鼠品系无关的普遍现象。确定导致HSV-1诱导的角膜瘢痕加重的gK诱导的免疫反应。
用gK对BALB/c或C57BL/6小鼠进行疫苗接种，用HSV-1 KOS株或McKrae株进行眼部攻击，并在攻击后28天确定角膜瘢痕的相对量。从接种gK的小鼠中分离出的T细胞、全血清或纯化的免疫球蛋白G（IgG）分别转移到未免疫的小鼠中，并确定HSV-1攻击后对角膜瘢痕的影响。
接种gK的BALB/c小鼠受到KOS攻击后导致显著的角膜瘢痕形成（P = 0.0003），尽管KOS通常不会导致角膜瘢痕形成。接种gK的C57BL/6小鼠受到McKrae攻击后导致显著的角膜瘢痕形成（P < 0.0001），尽管C57BL/6小鼠通常对HSV-1诱导的角膜瘢痕形成具有抗性。将抗gK小鼠全血清或纯化的抗gK小鼠IgG被动转移，但不是将抗gK T细胞的过继转移到未免疫的小鼠中，导致HSV-1攻击后角膜瘢痕加重（P < 0.0001）。T细胞依赖性抗体产生缺陷的小鼠对接种gK导致的HSV-1诱导的角膜瘢痕加重不敏感（P < 0.0001）。
接种gK加重HSV-1诱导的角膜瘢痕形成的能力并非小鼠品系或HSV-1毒株特异性的。gK诱导的角膜瘢痕加重与抗gK IgG有关。抗gK IgG如何加重HSV-1诱导的角膜瘢痕形成仍有待确定。
