Data on the expression of CXCR3 ligands and pro-inflammatory cytokines in macrophages and CD4+ T cells after stimuli of CXCR3 ligands
Bongjun Kim,
Jong-Ho Lee,
Won Jong Jin,
Hong-Hee Kim,
Hyunil Ha,
Zang Hee Lee
Affiliations
Bongjun Kim
Department of Cell and Developmental Biology, Dental Research Institute, School of Dentistry, Seoul National University, Seoul 110-749, Republic of Korea
Jong-Ho Lee
The University of Texas MD Anderson Cancer Center, Department of Neuro-Oncology, Huston, TX 77030, USA
Won Jong Jin
Department of Cell and Developmental Biology, Dental Research Institute, School of Dentistry, Seoul National University, Seoul 110-749, Republic of Korea
Hong-Hee Kim
Department of Cell and Developmental Biology, Dental Research Institute, School of Dentistry, Seoul National University, Seoul 110-749, Republic of Korea
Hyunil Ha
Clinical Research Division, Korea Institute of Oriental Medicine, 483 Expo-Ro, Yuseong-Gu, Daejeon 305-811, Republic of Korea; Corresponding author. Fax: +82 42 868 9668.
Zang Hee Lee
Department of Cell and Developmental Biology, Dental Research Institute, School of Dentistry, Seoul National University, Seoul 110-749, Republic of Korea; Corresponding author. Fax: +82 02 747 6589.
C-X-C motif chemokine receptor 3 (CXCR3) is a G protein-coupled receptor for three ligands which are C-X-C motif chemokine 9 (CXCL9), CXCL10, and CXCL11 [1]. Previously we have reported that CXCL10 promotes pro-inflammatory cytokine expression, and forms positive feedback loop [2,3]. In the present study, we described mRNA expression of CXCL9 and CXCL11 under CXCL10 stimuli in the presence or absence of CXCR3 antagonist, JN-2 in bone marrow-derived macrophages (BMMs) and CD4+ T cells. In addition, we examined pro-inflammatory cytokine expression under CXCL9 or CXCL11 stimuli in BMMs and CD4+ T cells. Keywords: CXCR3, CXCL9, CXCL11, Cytokine
