Abstract
Original language | English |
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Pages (from-to) | 2419-2425 |
Number of pages | 7 |
Journal | Leukemia and Lymphoma |
Volume | 58 |
Issue number | 10 |
DOIs | |
Publication status | Published - 2017 |
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The inhibitory receptor toll interleukin-1R 8 (TIR8/IL-1R8/SIGIRR) is downregulated in chronic lymphocytic leukemia. / Vilia, MG; Fonte, E; Veliz Rodriguez, T; Tocchetti, M; Ranghetti, P; Scarfò, L; Papakonstantinou, N; Ntoufa, S; Stamatopoulos, K; Ghia, P; Muzio, M.
In: Leukemia and Lymphoma, Vol. 58, No. 10, 2017, p. 2419-2425.Research output: Contribution to journal › Article
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TY - JOUR
T1 - The inhibitory receptor toll interleukin-1R 8 (TIR8/IL-1R8/SIGIRR) is downregulated in chronic lymphocytic leukemia
AU - Vilia, MG
AU - Fonte, E
AU - Veliz Rodriguez, T
AU - Tocchetti, M
AU - Ranghetti, P
AU - Scarfò, L
AU - Papakonstantinou, N
AU - Ntoufa, S
AU - Stamatopoulos, K
AU - Ghia, P
AU - Muzio, M
PY - 2017
Y1 - 2017
N2 - Toll interleukin-1 receptor 8 (also known as TIR8, SIGIRR, or IL1R8) is a transmembrane receptor that inhibits inflammation. Accordingly, genetic inactivation of this protein exacerbates chronic inflammation and inflammation-associated tumors in mice. In particular, lack of TIR8 triggers leukemia progression in a mouse model of chronic lymphocytic leukemia (CLL), supporting its role as a novel tumor restrainer. The aim of this study was to measure the amount of TIR8 mRNA and protein in CLL cells, and to analyze its regulation of expression. Circulating leukemic cells expressed lower levels of TIR8 compared to normal B-lymphocytes. Treatment of CLL cells with Azacytidine restored higher levels of TIR8 suggesting that DNA methylation may be involved in modulating TIR8 expression, with implications for novel therapeutic strategies. © 2017 Informa UK Limited, trading as Taylor & Francis Group
AB - Toll interleukin-1 receptor 8 (also known as TIR8, SIGIRR, or IL1R8) is a transmembrane receptor that inhibits inflammation. Accordingly, genetic inactivation of this protein exacerbates chronic inflammation and inflammation-associated tumors in mice. In particular, lack of TIR8 triggers leukemia progression in a mouse model of chronic lymphocytic leukemia (CLL), supporting its role as a novel tumor restrainer. The aim of this study was to measure the amount of TIR8 mRNA and protein in CLL cells, and to analyze its regulation of expression. Circulating leukemic cells expressed lower levels of TIR8 compared to normal B-lymphocytes. Treatment of CLL cells with Azacytidine restored higher levels of TIR8 suggesting that DNA methylation may be involved in modulating TIR8 expression, with implications for novel therapeutic strategies. © 2017 Informa UK Limited, trading as Taylor & Francis Group
U2 - 10.1080/10428194.2017.1295142
DO - 10.1080/10428194.2017.1295142
M3 - Article
VL - 58
SP - 2419
EP - 2425
JO - Leukemia and Lymphoma
JF - Leukemia and Lymphoma
SN - 1042-8194
IS - 10
ER -