Herpes simplex keratitis and dendritic cells at the crossroads: lessons from the past and a view into the future.

Massachusetts Eye and Ear Infirmary, Boston, MA 02114, USA.
International Ophthalmology Clinics 02/2009; 49(1):53-62. DOI: 10.1097/IIO.0b013e3181924dd8
Source: PubMed
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    ABSTRACT: To determine corneal sensitivity to selective mechanical, chemical, and thermal (heat and cold) stimulation in patients with a history of herpes simplex virus (HSV) keratitis. Corneal sensitivity to different modalities of stimulus was determined in both eyes of 16 patients with unilateral HSV keratitis diagnosed 1 to 12 months before the study. On slit lamp examination, 13 HSV-affected eyes showed corneal scarring or opacities, and three had no signs of previous keratitis. Corneal sensitivity was determined with the Belmonte gas esthesiometer. Mechanical, chemical, heat, and cold stimuli were applied on the central cornea. Eyes from 10 healthy subjects served as controls. In all control and contralateral eyes, selective mechanical, chemical, heat, and cold stimulation evoked sensations of subjective intensity proportional to the magnitude of the applied stimulus. In one HSV patient, the affected cornea was unresponsive to all types of stimuli, four lost only corneal sensitivity to mechanical stimulation, and three lost only sensitivity to heat. Mechanical (P<0.005) and heat (P<0.05) thresholds were raised in HSV eyes, whereas thresholds for CO2 were not modified. Also, HSV subjects identified poorly the intensity of mechanical, chemical, and heat stimuli, whereas sensitivity to cold stimulation was unaffected. In eyes that had had HSV keratitis, corneal sensitivity to mechanical forces and heat was significantly impaired, suggesting that axonal damage and/or altered expression of membrane ion channels involved in transduction and membrane excitability affects primarily the mechano- and polymodal nociceptor terminals. Corneal cold-sensitive terminals remain largely unaffected.
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    ABSTRACT: Recurrent herpes stromal keratitis (HSK) is one of the leading causes of blindness in the developed world. Cyokines characteristic of Th1 cells (in particular IFN-γ and IL-2) have been shown to dominate in HSK in addition to mechanisms by nonspecific, antigen-independent effector cells such as neutrophils, basophils, and monocytes. More recently, the migration and maturation of dendritic cells (DC) within the corneal stroma of patients with HSK have been recognized as contributors to recurrent disease, suggesting a role for delayed type hypersensitivity (DTH) in the immunopathogenesis of HSK. The role of DC and DTH in recurrent HSK has not been studied extensively and experimental models of recurrent HSK focusing on DTH as the pathogenesis and viral particles as the triggering antigen may contribute to better understanding of the disease.
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