May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Surface Expression of Glucocorticoid Induced TNF Receptor Family Related (GITR) Serves as a Marker for Non-Infectious Uveitis
Author Affiliations & Notes
  • S.P. Mahesh
    Laboratory of Immunology, NEI/NIH, Bethesda, MD, United States
  • Z. Li
    Laboratory of Immunology, NEI/NIH, Bethesda, MD, United States
  • R. Buggage
    Laboratory of Immunology, NEI/NIH, Bethesda, MD, United States
  • R.B. Nussenblatt
    Laboratory of Immunology, NEI/NIH, Bethesda, MD, United States
  • Footnotes
    Commercial Relationships  S.P. Mahesh, None; Z. Li, None; R. Buggage, None; R.B. Nussenblatt, None.
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 4605. doi:
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      S.P. Mahesh, Z. Li, R. Buggage, R.B. Nussenblatt; Surface Expression of Glucocorticoid Induced TNF Receptor Family Related (GITR) Serves as a Marker for Non-Infectious Uveitis . Invest. Ophthalmol. Vis. Sci. 2003;44(13):4605.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: To evaluate the expression of GITR ( Glucocorticoid Induced TNF Receptor Family Related) in peripheral blood lymphocytes in the normal population as well as in non-infectious uveitis patients. Methods: Peripheral blood mononuclear cells (PBMCs) were isolated from normal donors as well as from patients with non-infectious uveitis. Using a multiple color staining flow cytometry analysis procedure, GITR expression was studied in the various sub-populations of T cells. Results: In purified normal human PBMCs, GITR expression was low on resting CD4+ T cells while expression of GITR was highly increased in stimulated PBMCs. In normal human fresh blood, a small proportion of CD3+CD4+ T cells from normal donors constitutively expressed GITR. In addition, a higher percentage of GITR+ cells were observed among CD4+ CD25+ cells than in CD4+CD25- cells (p<0.01). In the non-infectious uveitis patient group, a significantly higher co-expression of GITR with CD25 was also observed (p<0.01). Interestingly, there was a significant increase of GITR expression in CD3+CD4+ T cells in uveitis patients compared to that in normal donors (p<0.01). This increased GITR expression was only seen in CD3+CD4+ T helper cells (p<0.01) but not in CD3+CD4- cytotoxic T cells. Also observed was the up regulation of GITR expression in CD3+CD4+ cells in active uveitis patients, which returned to normal when the patients disease became quiescent. Conclusions: GITR expression was seen in various subpopulations of T cells from normal donors and uveitis patients. It appeared to be preferentially co-expressed with CD25 in CD4+ T cells. GITR was upregulated in activated T cells as well as in CD3+ CD4+ T cells from non-infectious uveitis patients. The correlation of GITR expression with the disease course in non-infectious uveitis patients suggests that GITR may serve as a clinical marker for disease activity.

Keywords: uveitis-clinical/animal model • autoimmune disease • clinical laboratory testing 
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