Histaminergic regulation of interferon-gamma (IFN-γ) production by human natural killer (NK) cells

Asea, Alexzander; Hansson, Markus; Czerkinsky, Cécil; Houze, Thomas A.; Hermodsson, Svante; Strannegård, Örjan; Hellstrand, Kristoffer

doi:10.1046/j.1365-2249.1996.d01-755.x

Cited by 22 publications

(10 citation statements)

References 31 publications

(35 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This finding corroborates previous studies showing that superoxide radicals down-regulate most NK cell functions (22,23,(35)(36)(37)(38)(39). NK cells rapidly migrate to extravascular sites to attack and destroy altered target cells (40), and they are therefore especially important in controlling HSV infections in which the virus-infected cells otherwise escape CD8 ϩ T cell-mediated destruction as a consequence of the virus-induced downmodulation of MHC class I expression.…”

Section: Discussionsupporting

confidence: 91%

A Proinflammatory Peptide from Herpes Simplex Virus Type 2 Glycoprotein G Affects Neutrophil, Monocyte, and NK Cell Functions

Bellner

Thorén²,

Nygren

et al. 2005

The Journal of Immunology

View full text Add to dashboard Cite

We have identified a synthetic peptide derived from the secreted portion of HSV type 2 glycoprotein G, denoted gG-2p20, which has proinflammatory properties in vitro. The gG-2p20 peptide, corresponding to aa 190–205 of glycoprotein G-2, was a chemoattractant for both monocytes and neutrophils in a dose-dependent fashion, and also induced the release of reactive oxygen from these cells. The receptor mediating the responses was identified as the formyl peptide receptor. The gG-2p20-induced activation of phagocytes had a profound impact on NK cell functions. The reactive oxygen species produced by gG-2p20-activated phagocytes both inhibited NK cell cytotoxicity and accelerated the apoptotic cell death in NK cell-enriched lymphocyte populations. Hence, we have for the first time been able to identify a potential function of the secreted portion of HSV-2 glycoprotein G. We propose that the proinflammatory gG-2p20 peptide identified could contribute to a reduced function and viability of NK cells during HSV-2 infection due to its ability to recruit and activate phagocytic cells.

show abstract

Section: Discussionsupporting

confidence: 91%

A Proinflammatory Peptide from Herpes Simplex Virus Type 2 Glycoprotein G Affects Neutrophil, Monocyte, and NK Cell Functions

Bellner

Thorén²,

Nygren

et al. 2005

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…Functionally, CGD cells have been shown to display prolonged intracellular calcium transients upon stimulation, leading to exaggerated cellular responses [26]. ROS have also been implicated in numerous processes of potential importance for the inflammatory conditions displayed by CGD patients: neutrophil cell death (both apoptosis [27] and necrosis [28]), secondary clearance of apoptotic cells [29,30], and functional downregulation of immunocompetent lymphocytes [31]. In addition, rats with decreased capacity to produce ROS display increased susceptibility to autoimmune arthritis [32].…”

Section: Discussionmentioning

confidence: 99%

Enhanced inflammatory responses of chronic granulomatous disease leukocytes involve ROS‐independent activation of NF‐κB

et al. 2007

View full text Add to dashboard Cite

Reactive oxygen species (ROS) generated by the cellular NADPH-oxidase are crucial for phagocytic killing of ingested microbes and have been implicated as signaling molecules in various processes. For example, ROS are thought to be involved in activation of the transcription factor NF-jB, central for mediating production of proinflammatory cytokines in response to inflammatory stimuli. Several studies have demonstrated that inhibitors of the NADPH-oxidase interfere with NF-jB activation and production of proinflammatory cytokines. Curiously, patients with chronic granulomatous disease (CGD), an immunodeficiency characterized by an inability to produce ROS, are not only predisposed to severe infections, but also frequently develop various inflammatory complications indicative of exaggerated inflammatory responses. Here, we show that human CGD leukocytes display a hyperinflammatory phenotype with increased production of proinflammatory cytokines in response to stimulation with Toll-like receptor agonists. The hyperinflammatory phenotype was also evident in mononuclear cells from CGD mice (gp91 phox-/-), but not in control cells in the presence of NADPHoxidase inhibitor diphenyleneiodonium, probably reflecting NADPH-oxidase-independent effects of the inhibitor. Furthermore, we show that the major steps involved in NFjB activation were intact in human CGD cells. These data indicate that ROS were nonessential for activation of NF-jB and their production may even attenuate inflammation.

show abstract

“…Because IL-18 up-regulates perforin-mediated NK activity (46) and histamine was reported to enhance NK cell activity (47), it is possible that the effect of histamine on NK activity may be mediated by IL-18 secretion. Dohlsten et al (48) observed that histamine inhibited the production of IFN-␥ in activated PBMCs, while Asea et al reported that histamine enhanced the production of IFN-␥ in NK cells cocultured with monocytes by reducing monocytic production of reactive oxygen species (49). Both effects were reported to be mediated by H 2 receptors (48, 49), suggesting that H 2 receptors are present on many subsets of lymphocytes and that the stimulation of these receptors differentially regulates the production of IFN-␥ depending on the activation state of each subset.…”

Section: Discussionmentioning

confidence: 99%

Histamine Is a Potent Inducer of IL-18 and IFN-γ in Human Peripheral Blood Mononuclear Cells

Kohka

Nishibori²,

Ishibashi³

et al. 2000

The Journal of Immunology

View full text Add to dashboard Cite

Histamine (10−7 to 10−4 M) concentration-dependently stimulated the production of IL-18 and IFN-γ and inhibited the production of IL-2 and IL-10 in human PBMCs. Histamine in the same concentration range did not induce the production of IL-12 at all. The stimulatory or inhibitory effects of histamine on cytokine production were all antagonized by H2 receptor antagonists ranitidine and famotidine in a concentration-dependent manner, but not by H1 and H3 receptor antagonists. Selective H2 receptor agonists, 4-methylhistamine and dimaprit, mimicked the effects of histamine on five kinds of cytokine production. The EC50 values of histamine, 4-methylhistamine, and dimaprit for the production of IL-18 were 1.5, 1.0, and 3.8 μM, respectively. These findings indicated that histamine caused cytokine responses through the stimulation of H2 receptors. All effects of histamine on cytokine responses were also abolished by the presence of either anti-IL-18 Ab or IL-1β-converting enzyme/caspase-1 inhibitor, indicating that the histamine action is dependent on mature IL-18 secretion and that IL-18 production is located upstream of the cytokine cascade activated by histamine. The addition of recombinant human IL-18 to the culture concentration-dependently stimulated IL-12 and IFN-γ production and inhibited the IL-2 and IL-10 production. IFN-γ production induced by IL-18 was inhibited by anti-IL-12 Ab, showing the marked contrast of the effect of histamine. Thus histamine is a very important modulator of Th1 cytokine production in PBMCs and is quite unique in triggering IL-18-initiating cytokine cascade without inducing IL-12 production.

show abstract

Histaminergic regulation of interferon-gamma (IFN-γ) production by human natural killer (NK) cells

Cited by 22 publications

References 31 publications

A Proinflammatory Peptide from Herpes Simplex Virus Type 2 Glycoprotein G Affects Neutrophil, Monocyte, and NK Cell Functions

A Proinflammatory Peptide from Herpes Simplex Virus Type 2 Glycoprotein G Affects Neutrophil, Monocyte, and NK Cell Functions

Enhanced inflammatory responses of chronic granulomatous disease leukocytes involve ROS‐independent activation of NF‐κB

Histamine Is a Potent Inducer of IL-18 and IFN-γ in Human Peripheral Blood Mononuclear Cells

Contact Info

Product

Resources

About