Evidence for the immunosuppressive role of nicotine on human dendritic cell functions

Immunology. 2003 Jul;109(3):365-73. doi: 10.1046/j.1365-2567.2003.01655.x.


Nicotine alters a wide range of immunological functions, including innate and adaptive immune responses. To date, no studies have been reported showing the immunoregulatory effects of nicotine on dendritic cells (DCs), which are critical cells for initiation of cell-mediated immunity against infection and neoplastic diseases. In this work, we report that, in a nicotinic environment, monocyte-derived DCs manifest lower endocytic and phagocytic activities. Interestingly, although immature DCs undergo maturation in response to bacterial antigen lipopolysaccharide, they produce decreased levels of pro-inflammatory cytokines, notably interleukin-12, and reveal a reduced ability to stimulate antigen-presenting cell-dependent T-cell responses. Importantly, the reduction in T-cell responses is associated with a diminished ability of DCs to induce differentiation and expansion of type 1 T cells, as evidenced by a decreased frequency of interferon-gamma-producing effector cells. These results strongly suggest that nicotine can exert its immunosuppressive effects on immune surveillance through functional impairment of the DC system.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antigen Presentation / immunology
  • Cell Differentiation / drug effects
  • Cell Division / drug effects
  • Cells, Cultured
  • Cytokines / biosynthesis
  • Dendritic Cells / drug effects*
  • Dendritic Cells / immunology
  • Endocytosis / drug effects
  • Humans
  • Immune Tolerance / drug effects*
  • Lymphocyte Activation / drug effects
  • Nicotine / pharmacology*
  • Phagocytosis / drug effects
  • T-Lymphocytes / immunology


  • Cytokines
  • Nicotine