H1 histamine receptor antagonist inhibits constitutive growth of Jurkat T cells and antigen-specific proliferation of ovalbumin-specific murine T cells

Radvany, Zsuzsa; Darvas, Zsuzsanna; Kerekes, Krisztina; Prechl, József; Szalai, Csaba; Pállinger, Éva; László, Valéria; Varga, Valeria Lia; Sándor, Mátyás; Erdei, Anna; Falus, András

doi:10.1006/scbi.2000.0306

Cited by 34 publications

(24 citation statements)

References 11 publications

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“…Remarkably, other cells in the immune system which do not store histamine show high histidine decarboxylase activity and are capable of production of high amounts of histamine, which is secreted immediately after synthesis [37, 38]. These cells include platelets, monocytes/macrophages, DCs, neutrophils and T and B cells [39, 40]. …”

Section: Cellular Sources Of Histaminementioning

confidence: 99%

Histamine in Allergic Inflammation and Immune Modulation

Jutel¹,

Blaser²,

Akdiş³

2005

Int Arch Allergy Immunol

117

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Histamine, originally considered as a mediator of acute inflammatory and immediate hypersensitivity responses has also been demonstrated to affect chronic inflammation and regulate several essential events in the immune response. On the other hand, various cytokines control histamine synthesis, release and expression of histamine receptors (HRs). The cells involved in the regulation of immune response and hematopoiesis express HRs and also secrete histamine, which can selectively recruit the major effector cells into tissue sites and affect their maturation, activation, polarization and effector functions leading to chronic inflammation. Histamine, acting through its receptor type 2, positively interferes with the peripheral antigen tolerance induced by T regulatory cells in several pathways. Histamine also regulates antigen-specific Th1 and Th2 cells, as well as related antibody isotype responses. The diverse effects of histamine on immune regulation are due to differential expression and regulation of four HRs and their distinct intracellular signals. In addition, differences in affinities of these receptors are highly decisive on the biological effects of histamine and agents that target HRs. This article highlights the findings leading to a change of perspective in histamine immunobiology.

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Section: Cellular Sources Of Histaminementioning

confidence: 99%

Histamine in Allergic Inflammation and Immune Modulation

Jutel¹,

Blaser²,

Akdiş³

2005

Int Arch Allergy Immunol

117

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“…An alternative explanation would be that terfenadine and loratadine act on additional (undiscovered) HR or other molecular targets in neoplastic MC. Likewise, a number of previous and more recent data suggest that certain CYP450 isoenzymes serve as potential targets of terfenadine and loratadine and thus are mediating anti-neoplastic effects of these agents [22,[39][40][41][42][43]. If so, one could speculate that the other HR blockers tested did not interact with such enzymes in the same way or interact only with other CYP450 variants.…”

Section: Discussionmentioning

confidence: 96%

“…Another interesting concept is that histamine and histamine-metabolizing enzymes, both of which may interact with CYP450 isoenzymes, regulate the growth and survival of neoplastic cells in various tumors [39][40][41][42][43]. Some of these interactions may also point to autocrine or intercrine growth regulation in neoplastic cells [39][40][41][42][43].…”

Section: Discussionmentioning

confidence: 99%

“…Some of these interactions may also point to autocrine or intercrine growth regulation in neoplastic cells [39][40][41][42][43]. Since MC produce and contain considerable amounts of histamine it might be tempting to speculate that some of the HR blockers disrupt such autocrine or intercrine pathways involving histamine and histaminebinding molecules in neoplastic MC.…”

Section: Discussionmentioning

confidence: 99%

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H1-receptor antagonists terfenadine and loratadine inhibit spontaneous growth of neoplastic mast cells

Hadzijusufovic

Peter

Gleixner

et al. 2010

Experimental Hematology

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Objective-In mast cell (MC) neoplasms, clinical problems requiring therapy include i) the local aggressive and sometimes devastating growth of MC and ii) mediator-related symptoms. A key mediator of MC responsible for clinical symptoms is histamine. Therefore, the use of histamine receptor (HR) antagonists is an established approach to block histamine effects in these patients.Methods and Results-We screened for additional beneficial effects of HR antagonists and asked whether any of these agents would also exert growth-inhibitory effects on primary neoplastic MC, the human MC line HMC-1, and on two canine MC lines, C2 and NI-1. We found that the HR1 antagonists terfenadine and loratadine suppress spontaneous growth of HMC-1, C2, and NI-1 cells, as well as growth of primary neoplastic MC in all donors tested (human patients, n=5; canine patients, n=8). The effects of both drugs were found to be dose-dependent (IC 50 : terfenadine, 1-20 μM; loratadine, 10-50 μM). Both agents also produced apoptosis in neoplastic MC and augmented apoptosis-inducing effects of two KIT-targeting drugs, PKC412 and dasatinib. The other HR1 antagonists (fexofenadine, diphenhydramine) and HR2 antagonists (famotidine, cimetidine, ranitidine) tested did not exert substantial growth-inhibitory effects on neoplastic MC. None of the histamine receptor blockers were found to modulate cell cycle progression in neoplastic MC. Conclusions-The Europe PMC Funders Group Europe PMC Funders Author ManuscriptsEurope PMC Funders Author Manuscripts (terfenadine) alone or in combination with KIT-inhibitors, can also affect in vivo neoplastic MC growth remains to be determined.

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“…They can both secrete histamine and respond to histamine-induced activation of their HR [11][12][13]. One of the first techniques used to enrich histamine-bearing mononuclear cells was to precipitate histamine by binding to a protein conjugate which in turn was coupled to sepharose (H-RSA-S).…”

Section: Histamine Receptors On Lymphocytesmentioning

confidence: 99%

Histamine Receptors on Lymphocytes: Distribution and Functional Significance

Sachs

Hertl

Merk³

2000

Skin Pharmacol Physiol

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Several investigations reported modulation of lymphocyte functions following activation of the histamine H₂ receptor. However, few data have accumulated with regard to the distribution of histamine H₂ receptors on different lymphocyte subsets. Conversely, the distribution of histamine H₁ receptors on different lymphocyte subsets has been thoroughly analyzed using specific radioligands, whereas the functional significance of histamine H₁ receptor ligation on lymphocytes has not been fully elucidated yet. Recent investigations suggest that H₁R signaling on lymphocytes may enhance whereas activation of the H₂R may inhibit lymphocyte responses. In this review, the authors discuss the current knowledge on distribution and functional significance of histamine H₁ and histamine H₂ receptors on human lymphocytes.

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H1 histamine receptor antagonist inhibits constitutive growth of Jurkat T cells and antigen-specific proliferation of ovalbumin-specific murine T cells

Cited by 34 publications

References 11 publications

Histamine in Allergic Inflammation and Immune Modulation

Histamine in Allergic Inflammation and Immune Modulation

H1-receptor antagonists terfenadine and loratadine inhibit spontaneous growth of neoplastic mast cells

Histamine Receptors on Lymphocytes: Distribution and Functional Significance

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