|Cancer||Cell death||Cell cycle||Cytoskeleton||Exo/endocytosis||Differentiation||Division||Organelles||Signalling||Stem cells||Trafficking|
Cell Biology International (2011) 35, 9971000 (Printed in Great Britain)
Impact of histamine on dendritic cell functions
Tünde Simon*†1, Valéria László† and András Falus†‡
*Institute of Immunology, University of Debrecen, Debrecen, Hungary, †Department of Genetics, Cell and Immunobiology, Semmelweis University, Budapest, Hungary, and ‡Research Group for Inflammation Biology and Immunogenomics, Hungarian Academy of Sciences, Budapest, Hungary
A rapidly growing body of evidence highlighted that histamine, a small biogenic amine, is implicated in the regulation of DC (dendritic cell) functions. It is well established that DCs represent the most potent antigen-presenting cells of the body, linking innate and acquired immunity and regulating the outcome of immune responses. Signals, associated with ongoing inflammation and uptake of foreign antigens, promote maturation of DCs and activation of T-cell responses in secondary lymphatic organs. These bone marrow-derived cells patrol continuously all over the body. During their persistent migration, several mediators may influence the behaviour and functions of DCs. Histamine, produced by mast cells, basophils or DCs themselves, may have an important role in the life cycle of DCs. From the differentiation, through their never-ending circulation, until the induction of T-cell response, histamine is present and influences the life cycle of DCs. Here, we summarize recent progress in histamine research with respect to DC functions. We also point out some controversial aspects of histamine action on DCs.
Key words: antigen presentation, dendritic cell (DC) differentiation, histamine, migration, T-cell polarization
Abbreviations: DC, dendritic cell, H3R, H3 receptor, HDC, histidine decarboxylase, iDC, immature DC, IL, interleukin, IFNγ, interferon γ, LC, Langerhans cell, LPS, lipopolysaccharide, mDC, mature DC, OVA, ovalbumin, TLR, Toll-like receptor
1To whom correspondence should be addressed (email firstname.lastname@example.org).
Received 25 November 2010/13 February 2011; accepted 13 February 2011
Published online 31 August 2011, doi:10.1042/CBI20100844
© The Author(s) Journal compilation © 2011 Portland Press Limited