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Nicotine modulates the immunological function of dendritic cells through peroxisome proliferator-activated receptor-γ upregulation. | LitMetric

Nicotine modulates the immunological function of dendritic cells through peroxisome proliferator-activated receptor-γ upregulation.

Cell Immunol

Department of Periodontology, Division of Oral Biology and Disease Control, Osaka University Graduate School of Dentistry, Yamadaoka 1-8, Suita, Osaka 565-0871, Japan.

Published: June 2012

AI Article Synopsis

  • - The study investigated how nicotine affects the differentiation and functionality of dendritic cells (DCs), specifically human monocyte-derived DCs (NiDCs), finding that nicotine exposure led to decreased CD1a levels and suppressed secretion of key pro-inflammatory cytokines (IL-12 and TNF-α) in response to stimulation.
  • - NiDCs exhibited a weaker ability to promote the proliferation of T cells and produce IFN-γ, along with enhanced expression of molecules that inhibit immune responses (coinhibitory molecules), which suggests impaired immune activation.
  • - The research revealed that nicotine exposure increased levels of the nuclear receptor PPAR γ, which affects immune regulation, and that blocking a specific type of receptor (nACh

Article Abstract

We examined the effects of nicotine on differentiation and function of monocyte-derived human dendritic cells (DCs). NiDCs, which were the DCs differentiated in the presence of nicotine, showed lower levels of CD1a. Secretion of IL-12 and TNF-α by lipopolysaccharide (LPS)-stimulated NiDCs was significantly suppressed compared to monocyte-derived DCs grown without nicotine. NiDCs displayed a diminished capacity to induce allogeneic T cell proliferation with a reduced production of IFN-γ, and maintained/enhanced LPS-mediated expression of coinhibitory molecules. Interestingly, NiDCs enhanced the expression of nuclear receptor peroxisome proliferator-activated receptors γ (PPAR γ), which has immunomodulatory properties. Expression of PPAR γ and PPAR γ-target genes was significantly inhibited by pretreatment with d-tubocurarine, antagonist of non-selective nicotinic acetylcholine receptors (nAChR). In addition, reduction of Th1 responses was inhibited after blocking nAChR-mediated signal. These data suggest the effect of nicotine on altering DC immunogenicity by impeding Th1 immunity is partially mediated by upregulation of PPAR γ.

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Source
http://dx.doi.org/10.1016/j.cellimm.2012.02.007DOI Listing

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