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Dysfunction of CD4+CD25high T regulatory cells in patients with recurrent aphthous stomatitis.
J Oral Pathol Med. 2008 Sep; 37(8):454-61.JO

Abstract

BACKGROUND

Recurrent aphthous stomatitis (RAS) is a chronic inflammatory disease of unknown etiology characterized by recurring formation of painful oral ulcers. RAS may result from oral epithelium damage caused by T-cell-mediated immune response. CD4(+)CD25(+) T regulatory (Treg) cells suppress proliferation and effector functions of other immune cells, and therefore are crucial in regulating the immune response.

METHODS

We tested the function of peripheral CD4(+)CD25(high) Treg cells in active RAS through their ability to inhibit proliferation and cytokine production of conventional CD4(+) T cells. We also attempted to detect the presence of FOXP3 and indoleamine 2,3-dioxygenase (IDO) mRNA in the lesional and non-lesional oral mucosa of RAS patients and healthy individuals using real-time PCR assay.

RESULTS

Treg cells derived from RAS patients were less efficient in the suppression of cytokine production of CD4(+) T effector cells than Treg cells from healthy individuals. Moreover, in RAS, Treg cells were nearly twice less potent in the inhibition of CD4(+)CD25(-) T cell proliferation than in healthy donors. Furthermore, we have demonstrated the decreased proportion of CD4(+)CD25(+)FOXP3(+) Treg cells in peripheral blood of RAS patients compared with controls. We failed to detect FOXP3 mRNA, while IDO mRNA expression was decreased in non-lesional mucosa biopsies from RAS patients compared with ulcer biopsies or normal mucosa from healthy donors.

CONCLUSIONS

These findings suggest that CD4(+)CD25(high) Treg cells are both functionally and quantitatively compromised in RAS and that decreased constitutive expression of IDO in oral mucosa in RAS may lead to the loss of local immune tolerance.

Authors+Show Affiliations

Department of Periodontology and Oral Medicine, Medical University of Lodz, Lodz, Poland. natalewk@wp.plNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18318707

Citation

Lewkowicz, Natalia, et al. "Dysfunction of CD4+CD25high T Regulatory Cells in Patients With Recurrent Aphthous Stomatitis." Journal of Oral Pathology & Medicine : Official Publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology, vol. 37, no. 8, 2008, pp. 454-61.
Lewkowicz N, Lewkowicz P, Dzitko K, et al. Dysfunction of CD4+CD25high T regulatory cells in patients with recurrent aphthous stomatitis. J Oral Pathol Med. 2008;37(8):454-61.
Lewkowicz, N., Lewkowicz, P., Dzitko, K., Kur, B., Tarkowski, M., Kurnatowska, A., & Tchórzewski, H. (2008). Dysfunction of CD4+CD25high T regulatory cells in patients with recurrent aphthous stomatitis. Journal of Oral Pathology & Medicine : Official Publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology, 37(8), 454-61. https://doi.org/10.1111/j.1600-0714.2008.00661.x
Lewkowicz N, et al. Dysfunction of CD4+CD25high T Regulatory Cells in Patients With Recurrent Aphthous Stomatitis. J Oral Pathol Med. 2008;37(8):454-61. PubMed PMID: 18318707.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Dysfunction of CD4+CD25high T regulatory cells in patients with recurrent aphthous stomatitis. AU - Lewkowicz,Natalia, AU - Lewkowicz,Przemyslaw, AU - Dzitko,Katarzyna, AU - Kur,Barabara, AU - Tarkowski,Maciej, AU - Kurnatowska,Anna, AU - Tchórzewski,Henryk, Y1 - 2008/03/03/ PY - 2008/3/6/pubmed PY - 2009/1/27/medline PY - 2008/3/6/entrez SP - 454 EP - 61 JF - Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology JO - J. Oral Pathol. Med. VL - 37 IS - 8 N2 - BACKGROUND: Recurrent aphthous stomatitis (RAS) is a chronic inflammatory disease of unknown etiology characterized by recurring formation of painful oral ulcers. RAS may result from oral epithelium damage caused by T-cell-mediated immune response. CD4(+)CD25(+) T regulatory (Treg) cells suppress proliferation and effector functions of other immune cells, and therefore are crucial in regulating the immune response. METHODS: We tested the function of peripheral CD4(+)CD25(high) Treg cells in active RAS through their ability to inhibit proliferation and cytokine production of conventional CD4(+) T cells. We also attempted to detect the presence of FOXP3 and indoleamine 2,3-dioxygenase (IDO) mRNA in the lesional and non-lesional oral mucosa of RAS patients and healthy individuals using real-time PCR assay. RESULTS: Treg cells derived from RAS patients were less efficient in the suppression of cytokine production of CD4(+) T effector cells than Treg cells from healthy individuals. Moreover, in RAS, Treg cells were nearly twice less potent in the inhibition of CD4(+)CD25(-) T cell proliferation than in healthy donors. Furthermore, we have demonstrated the decreased proportion of CD4(+)CD25(+)FOXP3(+) Treg cells in peripheral blood of RAS patients compared with controls. We failed to detect FOXP3 mRNA, while IDO mRNA expression was decreased in non-lesional mucosa biopsies from RAS patients compared with ulcer biopsies or normal mucosa from healthy donors. CONCLUSIONS: These findings suggest that CD4(+)CD25(high) Treg cells are both functionally and quantitatively compromised in RAS and that decreased constitutive expression of IDO in oral mucosa in RAS may lead to the loss of local immune tolerance. SN - 1600-0714 UR - https://www.unboundmedicine.com/medline/citation/18318707/Dysfunction_of_CD4+CD25high_T_regulatory_cells_in_patients_with_recurrent_aphthous_stomatitis_ L2 - https://doi.org/10.1111/j.1600-0714.2008.00661.x DB - PRIME DP - Unbound Medicine ER -