Inhibition of effects of endogenously synthesized histamine disturbs in vitro human dendritic cell differentiation

Szeberényi, Júlia; Pállinger, Éva; Zsinkó, M.; Pós, Zoltán; Rothe, Gregor; Orsó, Evelyn; Szeberényi, Szabolcs; Schmitz, Gerd; Falus, András; László, Valéria

doi:10.1016/s0165-2478(01)00184-5

Cited by 79 publications

(56 citation statements)

References 24 publications

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“…6c), which was the adjuvant used in the mouse model. These results are consistent with previous studies suggesting that dendritic cells express HDC (28). To test the role of endogenous histamine production in this in vitro system, purified CD11c ϩ dendritic cells were cultured overnight with ␣-fluoromethyl histidine, a well-characterized HDC inhibitor.…”

Section: Decreased Allergic Airway Inflammation By H 4 R Antagonistssupporting

confidence: 90%

The Histamine H4 Receptor Mediates Allergic Airway Inflammation by Regulating the Activation of CD4+ T Cells

Dunford

O'Donnell

Riley

et al. 2006

The Journal of Immunology

263

302

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Histamine is an important inflammatory mediator that is released in airways during an asthmatic response. However, current antihistamine drugs are not effective in controlling the disease. The discovery of the histamine H4 receptor (H4R) prompted us to reinvestigate the role of histamine in pulmonary allergic responses. H4R-deficient mice and mice treated with H4R antagonists exhibited decreased allergic lung inflammation, with decreases in infiltrating lung eosinophils and lymphocytes and decreases in Th2 responses. Ex vivo restimulation of T cells showed decreases in IL-4, IL-5, IL-13, IL-6, and IL-17 levels, suggesting that T cell functions were disrupted. In vitro studies indicated that blockade of the H4R on dendritic cells leads to decreases in cytokine and chemokine production and limits their ability to induce Th2 responses in T cells. This work suggests that the H4R can modulate allergic responses via its influence on T cell activation. The study expands the known influences of histamine on the immune system and highlights the therapeutic potential of H4R antagonists in allergic conditions.

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Section: Decreased Allergic Airway Inflammation By H 4 R Antagonistssupporting

confidence: 90%

The Histamine H4 Receptor Mediates Allergic Airway Inflammation by Regulating the Activation of CD4+ T Cells

Dunford

O'Donnell

Riley

et al. 2006

The Journal of Immunology

263

302

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“…Histamine alone failed to induce the maturation of DCs, as shown by phenotypic analysis (Table 1); thus, histamine had no effect on the maturation marker CD83 or on CD40, although it did cause moderate but consistent increases in CD86, CD80, MHC II, and a slight decrease in MHC I. Small histamine-mediated effects on iDC phenotype have also been seen by others (33,34). Incubation of iDCs Incubation of iDCs with histamine causes an increase in intracellular calcium that is blocked by an H1-specific antagonist.…”

Section: Resultssupporting

confidence: 64%

Histamine regulates cytokine production in maturing dendritic cells, resulting in altered T cell polarization

Mazzoni¹,

Young²,

Spitzer³

et al. 2001

J. Clin. Invest.

274

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Atopic diseases such as allergy and asthma are characterized by increases in Th2 cells and serum IgE antibodies. The binding of allergens to IgE on mast cells triggers the release of several mediators, of which histamine is the most prevalent. Here we show that histamine, together with a maturation signal, acts directly upon immature dendritic cells (iDCs), profoundly altering their T cell polarizing capacity. We demonstrate that iDCs express two active histamine receptors, H1 and H2. Histamine did not significantly affect the LPS-driven maturation of iDCs with regard to phenotypic changes or capacity to prime naive T cells, but it dramatically altered the repertoire of cytokines and chemokines secreted by mature DCs. In particular, histamine, acting upon the H2 receptor for a short period of time, increased IL-10 production and reduced IL-12 secretion. As a result, histamine-matured DCs polarized naive CD4 + T cells toward a Th2 phenotype, as compared with DCs that had matured in the absence of histamine. We propose that the Th2 cells favor IgE production, leading to increased histamine secretion by mast cells, thus creating a positive feedback loop that could contribute to the severity of atopic diseases.

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“…More recent studies have shown that histamine is also able to modulate the function of DCs. Histamine appears to be involved in the normal differentiation of human DCs (19), and it is also capable of inducing the chemotaxis of immature DCs (20) and promoting the differentiation of T CD4 ϩ cells into a Th2 profile (21,22), a mechanism that seems to contribute to the severity of atopic diseases.…”

Section: Endritic Cells (Dcs)mentioning

confidence: 99%

Histamine Improves Antigen Uptake and Cross-Presentation by Dendritic Cells

Amaral

Davio

Ceballos

et al. 2007

The Journal of Immunology

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Previous studies have shown that histamine is able to modulate the function of dendritic cells (DCs). Histamine seems to be required for the normal differentiation of DCs. Moreover, it is capable of stimulating the chemotaxis of immature DCs and of promoting the differentiation of T CD4+ cells into a Th2 profile. In this study, we analyzed whether histamine was able to modulate endocytosis and cross-presentation mediated by immature DCs. Our results show that both functions are stimulated by histamine. Endocytosis of soluble HRP and FITC-OVA and cross-presentation of soluble OVA were markedly increased by histamine. Interestingly, stimulation of endocytosis and cross-presentation appeared to be mediated through different histamine receptors. In fact, the enhancement of endocytosis was prevented by the histamine2 receptor (H2R) antagonist cimetidine, whereas the stimulation of cross-presentation was prevented by the H3R/H4R antagonist thioperamide. Of note, contrasting with the observations made with soluble Ags, we found that histamine did not increase either the uptake of OVA-attached to latex beads, or the cross-presentation of OVA immobilized on latex beads. This suggests that the ability of histamine to increase endocytosis and cross-presentation is dependent on the Ag form and/or the mechanisms through which the Ag is internalized by DCs. Our results support that histamine may favor cross-presentation of soluble allergens by DCs enabling the activation of allergen-specific T CD8+ cells, which appears to play an important role in the development of allergic responses in the airway.

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Inhibition of effects of endogenously synthesized histamine disturbs in vitro human dendritic cell differentiation

Cited by 79 publications

References 24 publications

The Histamine H4 Receptor Mediates Allergic Airway Inflammation by Regulating the Activation of CD4+ T Cells

The Histamine H4 Receptor Mediates Allergic Airway Inflammation by Regulating the Activation of CD4+ T Cells

Histamine regulates cytokine production in maturing dendritic cells, resulting in altered T cell polarization

Histamine Improves Antigen Uptake and Cross-Presentation by Dendritic Cells

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