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Suppression of interleukin-17-producing T-helper 17 cells by retinal pigment epithelial cells.
Jpn J Ophthalmol. 2011 Sep; 55(5):565-575.JJ

Abstract

PURPOSE

To determine whether retinal pigment epithelial (RPE) cells can inhibit cytokine production by activated T helper (Th) cells.

METHODS

Primary RPE cells were cultured from normal C57BL/6 mice. Target bystander T cells were established from normal splenic T cells with anti-CD3 antibodies. T-cell activation was assessed for production of cytokines, determined by ELISA. Production of IL-17 on target T cells was evaluated using oligonucleotide microarray, RT-PCR and flow cytometry. TGFβ small interfering RNA was used to inhibit the RPE cells' inhibitory function.

RESULTS

The cultured RPE cells greatly suppressed the activation of bystander CD4(+) T cells in vitro, especially cytokine production by target T helper cells (Th1 cells, Th2 cells and Th17 cells, but not Th3 cells). The cultured RPE cells and RPE supernatants significantly suppressed the IL-17-producing CD4(+) T cells and fully suppressed the polarized Th17 cell lines that were induced by recombinant proteins IL-6 and TGFβ2. However, the RPE cells failed to suppress the IL-17-producing T cells in the presence of rIL-6. In addition, the TGFβ produced by the RPE cells suppressed the Th17 cells.

CONCLUSIONS

These results indicate that RPE cells have an immunosuppressive effect on Th17-type effector T cells, which highlights a role for ocular resident cells in establishing immune regulation in the eye.

Authors+Show Affiliations

Department of Ophthalmology and Visual Science, Tokyo Medical and Dental University Graduate School of Medicine, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8519, Japan. sunaoph@tmd.ac.jp.Department of Ophthalmology and Visual Science, Tokyo Medical and Dental University Graduate School of Medicine, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8519, Japan.Department of Ophthalmology and Visual Science, Tokyo Medical and Dental University Graduate School of Medicine, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8519, Japan.Department of Ophthalmology and Visual Science, Tokyo Medical and Dental University Graduate School of Medicine, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8519, Japan.Department of Ophthalmology and Visual Science, Tokyo Medical and Dental University Graduate School of Medicine, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8519, Japan.Department of Ophthalmology and Visual Science, Tokyo Medical and Dental University Graduate School of Medicine, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8519, Japan.

Pub Type(s)

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

Language

eng

PubMed ID

21750969

Citation

Sugita, Sunao, et al. "Suppression of Interleukin-17-producing T-helper 17 Cells By Retinal Pigment Epithelial Cells." Japanese Journal of Ophthalmology, vol. 55, no. 5, 2011, pp. 565-575.
Sugita S, Horie S, Yamada Y, et al. Suppression of interleukin-17-producing T-helper 17 cells by retinal pigment epithelial cells. Jpn J Ophthalmol. 2011;55(5):565-575.
Sugita, S., Horie, S., Yamada, Y., Kawazoe, Y., Takase, H., & Mochizuki, M. (2011). Suppression of interleukin-17-producing T-helper 17 cells by retinal pigment epithelial cells. Japanese Journal of Ophthalmology, 55(5), 565-575. https://doi.org/10.1007/s10384-011-0064-9
Sugita S, et al. Suppression of Interleukin-17-producing T-helper 17 Cells By Retinal Pigment Epithelial Cells. Jpn J Ophthalmol. 2011;55(5):565-575. PubMed PMID: 21750969.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Suppression of interleukin-17-producing T-helper 17 cells by retinal pigment epithelial cells. AU - Sugita,Sunao, AU - Horie,Shintaro, AU - Yamada,Yukiko, AU - Kawazoe,Yuko, AU - Takase,Hiroshi, AU - Mochizuki,Manabu, Y1 - 2011/07/13/ PY - 2010/11/25/received PY - 2011/04/19/accepted PY - 2011/7/14/entrez PY - 2011/7/14/pubmed PY - 2012/1/6/medline SP - 565 EP - 575 JF - Japanese journal of ophthalmology JO - Jpn J Ophthalmol VL - 55 IS - 5 N2 - PURPOSE: To determine whether retinal pigment epithelial (RPE) cells can inhibit cytokine production by activated T helper (Th) cells. METHODS: Primary RPE cells were cultured from normal C57BL/6 mice. Target bystander T cells were established from normal splenic T cells with anti-CD3 antibodies. T-cell activation was assessed for production of cytokines, determined by ELISA. Production of IL-17 on target T cells was evaluated using oligonucleotide microarray, RT-PCR and flow cytometry. TGFβ small interfering RNA was used to inhibit the RPE cells' inhibitory function. RESULTS: The cultured RPE cells greatly suppressed the activation of bystander CD4(+) T cells in vitro, especially cytokine production by target T helper cells (Th1 cells, Th2 cells and Th17 cells, but not Th3 cells). The cultured RPE cells and RPE supernatants significantly suppressed the IL-17-producing CD4(+) T cells and fully suppressed the polarized Th17 cell lines that were induced by recombinant proteins IL-6 and TGFβ2. However, the RPE cells failed to suppress the IL-17-producing T cells in the presence of rIL-6. In addition, the TGFβ produced by the RPE cells suppressed the Th17 cells. CONCLUSIONS: These results indicate that RPE cells have an immunosuppressive effect on Th17-type effector T cells, which highlights a role for ocular resident cells in establishing immune regulation in the eye. SN - 1613-2246 UR - https://www.unboundmedicine.com/medline/citation/21750969/Suppression_of_interleukin_17_producing_T_helper_17_cells_by_retinal_pigment_epithelial_cells_ L2 - https://dx.doi.org/10.1007/s10384-011-0064-9 DB - PRIME DP - Unbound Medicine ER -