Histamine regulates T-cell and antibody responses by differential expression of H1 and H2 receptors
Marek Jutel (),
Takeshi Watanabe,
Sven Klunker,
Mübeccel Akdis,
Olivier A. R. Thomet,
Jozef Malolepszy,
Teresa Zak-Nejmark,
Ritsuko Koga,
Takashi Kobayashi,
Kurt Blaser and
Cezmi A. Akdis ()
Additional contact information
Marek Jutel: Swiss Institute of Allergy and Asthma Research (SIAF)
Takeshi Watanabe: Medical Institute of Bioregulation, Kyushu University
Sven Klunker: Swiss Institute of Allergy and Asthma Research (SIAF)
Mübeccel Akdis: Swiss Institute of Allergy and Asthma Research (SIAF)
Olivier A. R. Thomet: Swiss Institute of Allergy and Asthma Research (SIAF)
Jozef Malolepszy: Wroclaw Medical University
Teresa Zak-Nejmark: Wroclaw Medical University
Ritsuko Koga: Medical Institute of Bioregulation, Kyushu University
Takashi Kobayashi: Medical Institute of Bioregulation, Kyushu University
Kurt Blaser: Swiss Institute of Allergy and Asthma Research (SIAF)
Cezmi A. Akdis: Swiss Institute of Allergy and Asthma Research (SIAF)
Nature, 2001, vol. 413, issue 6854, 420-425
Abstract:
Abstract Many pathological processes, including those causing allergies and autoimmune diseases, are associated with the presence of specialized subsets of T helper cells (TH1 and TH2) at the site of inflammation1,2,3,4. The diversity of TH1 and TH2 function is not predetermined but depends on signals that drive the cells towards either subset1,2,3,4. Histamine, released from effector cells (mast cells and basophils) during inflammatory reactions can influence immune response5,6,7,8. Here we report that histamine enhances TH1-type responses by triggering the histamine receptor type 1 (H1R), whereas both TH1- and TH2-type responses are negatively regulated by H2R through the activation of different biochemical intracellular signals. In mice, deletion of H1R results in suppression of interferon (IFN)-γ and dominant secretion of TH2 cytokines (interleukin (IL)-4 and IL-13). Mutant mice lacking H2R showed upregulation of both TH1 and TH2 cytokines. Relevant to T-cell cytokine profiles, mice lacking H1R displayed increased specific antibody response with increased immunoglobulin-ε (IgE) and IgG1, IgG2b and IgG3 compared with mice lacking H2R. These findings account for an important regulatory mechanism in the control of inflammatory functions through effector-cell-derived histamine.
Date: 2001
References: Add references at CitEc
Citations:
Downloads: (external link)
https://www.nature.com/articles/35096564 Abstract (text/html)
Access to the full text of the articles in this series is restricted.
Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.
Export reference: BibTeX
RIS (EndNote, ProCite, RefMan)
HTML/Text
Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:413:y:2001:i:6854:d:10.1038_35096564
Ordering information: This journal article can be ordered from
https://www.nature.com/
DOI: 10.1038/35096564
Access Statistics for this article
Nature is currently edited by Magdalena Skipper
More articles in Nature from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().