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Role of Thalidomide on the Expression of OX40, 4-1BB, and GITR in T Cell Subsets.
Kim, B S; Kim, J Y; Kim, E J; Lee, J G; Joo, D J; Huh, K H; Kim, M S; Kim, Y S.
Afiliación
  • Kim BS; The Research Institute for Transplantation, Yonsei University College of Medicine Seoul, Republic of Korea; Division of Nephrology, Department of Internal Medicine Severance Hospital, Yonsei University Health System, Seoul, Republic of Korea.
  • Kim JY; The Research Institute for Transplantation, Yonsei University College of Medicine Seoul, Republic of Korea.
  • Kim EJ; The Research Institute for Transplantation, Yonsei University College of Medicine Seoul, Republic of Korea; Brain Korea 21 PLUS Project for Medical Science, Yonsei University, Seoul, Republic of Korea.
  • Lee JG; The Research Institute for Transplantation, Yonsei University College of Medicine Seoul, Republic of Korea; Department of Transplantation Surgery, Severance Hospital, Yonsei University Health System, Seoul, Republic of Korea.
  • Joo DJ; The Research Institute for Transplantation, Yonsei University College of Medicine Seoul, Republic of Korea; Department of Transplantation Surgery, Severance Hospital, Yonsei University Health System, Seoul, Republic of Korea.
  • Huh KH; The Research Institute for Transplantation, Yonsei University College of Medicine Seoul, Republic of Korea; Department of Transplantation Surgery, Severance Hospital, Yonsei University Health System, Seoul, Republic of Korea.
  • Kim MS; The Research Institute for Transplantation, Yonsei University College of Medicine Seoul, Republic of Korea; Department of Transplantation Surgery, Severance Hospital, Yonsei University Health System, Seoul, Republic of Korea.
  • Kim YS; The Research Institute for Transplantation, Yonsei University College of Medicine Seoul, Republic of Korea; Department of Transplantation Surgery, Severance Hospital, Yonsei University Health System, Seoul, Republic of Korea. Electronic address: yukim@yuhs.ac.
Transplant Proc ; 48(4): 1270-4, 2016 May.
Article en En | MEDLINE | ID: mdl-27320601
BACKGROUND: Thalidomide (TM) is known to have anti-cancer and anti-inflammatory properties; however, its mechanism on T cells is still unclear. We previously showed the immune modulatory effect of TM on T cells and its therapeutic effect on lupus nephritis models. Here we examined the changes in the expression of tumor necrosis factor receptor superfamilies (TNFRSFs), including OX40, 4-1BB, and glucocorticoid-induced TNFR-related protein (GITR) in T cell subsets by TM treatments. METHODS: Splenic naïve T cells (Tnaives) from C57BL/6 mice were sort-purified and cultured for CD4(+) T cell proliferation and regulatory T cells (Tregs) conversion with TM treatments. All samples were analyzed by flow cytometry after stained with anti-mouse CD4, Foxp3, OX40, 4-1BB, or GITR antibodies. RESULTS: Expressions of OX40, 4-1BB, and GITR on CD4(+) T cells showed a decreasing tendency by TM treatments. Especially, downregulation of these molecules on CD4(+)CFSE(low) T cells was significant in TM treatment groups. On the condition of Treg conversion, OX40 was downregulated significantly. In contrast, the expression of GITR was increased, and that of 4-1BB had shown no particular change under the condition of Treg. CONCLUSION: Considering these results, TM may have an immune modulatory role through the T cell subset-specific change of OX40, 4-1BB, and GITR expression. Further study is required to elucidate the effect of thalidomide on T cells.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Talidomida / Subgrupos de Linfocitos T / Ligando 4-1BB / Proteína Relacionada con TNFR Inducida por Glucocorticoide / Receptores OX40 / Inmunosupresores Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Transplant Proc Año: 2016 Tipo del documento: Article Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Talidomida / Subgrupos de Linfocitos T / Ligando 4-1BB / Proteína Relacionada con TNFR Inducida por Glucocorticoide / Receptores OX40 / Inmunosupresores Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Transplant Proc Año: 2016 Tipo del documento: Article Pais de publicación: Estados Unidos