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August 1981

Lymphocyte Transformation in Presumed Ocular Histoplasmosis

Author Affiliations

From the Department of Ophthalmology, Louisiana State University School of Medicine, Shreveport (Dr Ganley); The National Institute of Neurological Diseases, Communicative Disorders, and Stroke, National Institutes of Health, Bethesda, Md (Drs Nemo and Brody); and the Department of Epidemiology, School of Hygiene and Public Health, The Johns Hopkins University, Baltimore, (Dr Comstock).

Arch Ophthalmol. 1981;99(8):1424-1429. doi:10.1001/archopht.1981.03930020298021

• Lymphocytes from individuals with inactive macular disciform lesions of presumed ocular histoplasmosis challenged with three histoplasmin antigens incorporated tritiated thymidine at a significantly higher rate than histoplasmin-stimulated lymphocytes of matched control and peripheral scar groups. This finding is consistent with the etiologic association of the disciform ocular syndrome and previous systemic infection with Histoplasma capsulatum. The disciform group had a higher mean response than the other two groups to pokeweed mitogen but not to phytohemagglutinin and had higher mean counts per minute to the specific antigens Toxoplasma gondii, Blastomyces dermatitidis, Cryptococcus neoformans, Mycobacterium tuberculosis, M battey, and M gaus, but not to Candida albicans. These data would suggest that individuals with the disciform lesion of presumed ocular histoplasmosis have a hyperreactive cellular immune response; this response may play an important role in the development of the disciform lesion.

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