title: Irisflorentin modifies properties of mouse bone marrow-derived dendritic cells and reduces the allergic contact hypersensitivity responses.
abstract: Irisflorentin is an isoflavone component derived from the roots of Belamcanda chinensis (L.) DC. In traditional Chinese medicine, this herb has pharmacological properties to treat inflammatory disorders. Dendritic cells (DCs) are crucial modulators for the development of optimal T-cell immunity and maintenance of tolerance. Aberrant activation of DCs can induce harmful immune responses, and so agents that effectively improve DC properties have great clinical value. We herein investigated the effects of irisflorentin on lipopolysaccharide (LPS)-stimulated maturation of mouse bone marrow-derived DCs in vitro and in the contact hypersensitivity response (CHSR) in vivo. Our results demonstrated that treatment with up to 40 μM irisflorentin does not cause cellular toxicity. Irisflorentin significantly lessened the proinflammatory cytokine production (tumor necrosis factor-α, interleukin-6, and interleukin-12p70) by LPS-stimulated DCs. Irisflorentin also inhibited the expression of LPS-induced major histocompatibility complex class II and costimulatory molecules (CD40 and CD86) on LPS-stimulated DCs. In addition, irisflorentin diminished LPS-stimulated DC-elicited allogeneic T-cell proliferation. Furthermore, irisflorentin significantly interfered with LPS-induced activation of IκB kinase, c-Jun N-terminal kinase, and p38, as well as the nuclear translocation of NF-κB p65. Subsequently, treatment with irisflorentin obviously weakened 2,4-dinitro-1-fluorobenzene-induced delayed-type hypersensitivity. These findings suggest new insights into the role of irisflorentin as an immunotherapeutic adjuvant through its capability to modulate the properties of DCs.
authors: Graduate Institute of Immunology, China Medical University, Taichung, Taiwan.
authors: Ru-Huei
authors: RH
authors: Fu
authors: Chia-Wen
authors: CW
authors: Tsai
authors: Rong-Tzong
authors: RT
authors: Tsai
authors: Shih-Ping
authors: SP
authors: Liu
authors: Tzu-Min
authors: TM
authors: Chan
authors: Yu-Chen
authors: YC
authors: Ho
authors: Hsin-Lien
authors: HL
authors: Lin
authors: Yue-Mi
authors: YM
authors: Chen
authors: Huey-Shan
authors: HS
authors: Hung
authors: Shao-Chih
authors: SC
authors: Chiu
authors: Chang-Hai
authors: CH
authors: Tsai
authors: Yu-Chi
authors: YC
authors: Wang
authors: Woei-Cherng
authors: WC
authors: Shyu
authors: Shinn-Zong
authors: SZ
authors: Lin
mesh_terms: D000818:Animals; D051940:B7-2 Antigen / Q000378:metabolism; D001854:Bone Marrow Cells / Q000166:cytology; D019013:CD40 Antigens / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D003713:Dendritic Cells / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D003877:Dermatitis, Contact / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D000949:Histocompatibility Antigens Class II / Q000378:metabolism; D051550:I-kappa B Kinase / Q000378:metabolism; D027621:Iridaceae / Q000737:chemistry / Q000378:metabolism; D007529:Isoflavones / Q000737:chemistry / Q000494:pharmacology* / Q000627:therapeutic use; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D008516:Medicine, Chinese Traditional; D051379:Mice; D008810:Mice, Inbred C57BL; D010766:Phosphorylation / Q000187:drug effects; D018517:Plant Roots / Q000737:chemistry / Q000378:metabolism; D051996:Transcription Factor RelA / Q000378:metabolism; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D051940:B7-2 Antigen; D019013:CD40 Antigens; D016207:Cytokines; D000949:Histocompatibility Antigens Class II; D007529:Isoflavones; D008070:Lipopolysaccharides; D051996:Transcription Factor RelA; C570745:irisflorentin; D051550:I-kappa B Kinase; D048031:JNK Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases