Roles of TNF-α and IgE in the late phase of contact hypersensitivity induced by trimellitic anhydride

Chai, Ok Hee; Lee, Hern Ku; Lee, Yong Chul; Lee, Moo Sam; Han, Eugene; Kim, Hyoung Tae; Song, Chang Ho

doi:10.1038/emm.2005.51

Cited by 12 publications

(13 citation statements)

References 32 publications

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“…Also, TNF-α is a chemotactic cytokine for granulocytes (Sabatini et al, 2002;Chai et al, 2005;Yoshifuku et al, 2007), probably by up-regulation of cellular adhesion molecules, such as E-selectin, ICAM-1 and VCAM-1, thus facilitating migration of eosinophils and neutrophils. During this process, they also become primed for mediator secretion.…”

Section: Discussionmentioning

confidence: 99%

“…Mast cell-derived lipid mediators and inflammatory cytokines, such as leukotrienes, IL-6, and TNF-α, have also been reported to play an important role in the late asthmatic response and airway hyperresponsiveness (Matsuoka et al, 2000; Zimmermann et al, 2003;Antunez et al, 2006;Woodruff et al, 2009). TNF-α is a chemotactic cytokine for granulocytes, including eosinophils and neutrophils (Sabatini et al, 2002;Chai et al, 2005;Yoshifuku et al, 2007), probably by upregulation of cellular adhesion molecules, such as vascular cellular adhesion molecule (VCAM)-1, and intercellular adhesion molecule (ICAM)-1, thus facilitating migration of eosinophils and neutrophils. During this process, they also become primed for mediator secretion.…”

Section: Introductionmentioning

confidence: 99%

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Mast cells play a key role in Th2 cytokine-dependent asthma model through production of adhesion molecules by liberation of TNF-α

et al. 2011

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mast cells play a key role in Th2 cytokine-dependent asthma model through production of adhesion molecules by liberation of TNF-α

et al. 2011

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“…This observation is extremely important, because MCP-1, MIP-1␣, and TNF-␣ are known to play crucial roles in the pathogenesis of contact dermatitis. For example, the ear swelling following a challenge with oxazolone was diminished in TNF-␣-deficient mice (43)(44)(45)(46), and the recruitment of mononuclear cells was impaired in MCP-1-deficient mice (47). Thus, it seems possible that the CB2 receptor and its endogenous ligand 2-AG participate in the elicitation phase of contact dermatitis by up-regulating the production of these cytokines.…”

Section: Discussionmentioning

confidence: 99%

Involvement of the Cannabinoid CB2 Receptor and Its Endogenous Ligand 2-Arachidonoylglycerol in Oxazolone-Induced Contact Dermatitis in Mice

Oka

Wakui

Ikeda

et al. 2006

The Journal of Immunology

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The possible involvement of 2-arachidonoylglycerol (2-AG), an endogenous ligand for the cannabinoid receptors (CB1 and CB2), in contact dermatitis in mouse ear was investigated. We found that the level of 2-AG was markedly elevated in the ear following a challenge with oxazolone in sensitized mice. Of note, the swelling following the challenge was suppressed by either the administration of SR144528, a CB2 receptor antagonist, immediately after sensitization, or the administration of SR144528 upon the challenge. The effect of AM251, a CB1 receptor antagonist, was marginal in either case. It seems apparent, therefore, that the CB2 receptor and its endogenous ligand 2-AG are closely involved in both the sensitization phase and the elicitation phase of oxazolone-induced contact dermatitis. In line with this, we found that Langerhans cells (MHC class II+) contain a substantial amount of CB2 receptor mRNA, whereas keratinocytes (MHC class II−) do not. We also obtained evidence that the expression of mRNAs for proinflammatory cytokines following a challenge with oxazolone was markedly suppressed by treatment with SR144528. We next examined whether the CB2 receptor and 2-AG participate in chronic contact dermatitis accompanied by the infiltration of tissues by eosinophils. The amount of 2-AG in mouse ear dramatically increased following repeated challenge with oxazolone. Importantly, treatment with SR144528 attenuated both the recruitment of eosinophils and ear swelling in chronic contact dermatitis induced by repeated challenge with oxazolone. These results strongly suggest that the CB2 receptor and 2-AG play important stimulative roles in the sensitization, elicitation, and exacerbation of allergic inflammation.

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“…Bulk splenocytes after LPS stimulation from LT −/− mice produced a four-fold increase in IL-12 compared to cells from WT mice and similarly, collagenase digested lung cells also had a threefold increase in IL-12 production (285 ± 38.7 pg/ml from LT−/− and 85.9 ± 3.8 pg/ml from WT, P=0.0014). IgE neutralization with non-anaphylactic anti-IgE has been used to examine the role of IgE in immediate and late responses in allergic airway inflammation, late phases of contact hypersensitivity, airway responses in respiratory syncitial virus, behavioral correlates and ulcerative colitis [24; 25; 26; 27; 28]. Monoclonal antibodies neutralize free serum IgE without crosslinking IgE bound to mast cells therefore, reducing the overall serum level of IgE without triggering mast cell mediated events such as histamine, leukotriene and cytokine release.…”

Section: Resultsmentioning

confidence: 99%

IgE regulates T helper cell differentiation through FcγRIII mediated dendritic cell cytokine modulation

Blink

2010

Cellular Immunology

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Asthma and allergy are characterized by dysregulation of inflammatory responses toward Th2 responses and high serum levels of IgE. IgE plays a role in the effector phase by triggering the degranulation of mast cells after antigen-cross-linking but its role in the induction of helper T cell differentiation is unknown. We have previously shown lymphotoxin is required for maintaining physiological levels of serum IgE which minimize spontaneous Th1-mediated airway inflammation, suggesting a physiological role for IgE in the regulation of T helper cell differentiation. We describe the mechanism in which IgE modulates inflammation by regulating dendritic cell cytokine production. Physiological levels of IgE suppress IL-12 production in the spleen and lung, suggesting IgE limits Th1 responses in vivo. IgE directly stimulates dendritic cells through FcγRIII to suppress IL-12 in vitro and influences APC to skew CD4+ T cells toward Th2 differentiation. We demonstrate a novel role for IgE in regulating differentiation of adaptive inflammatory responses through direct interaction with FcγRIII on dendritic cells.

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Roles of TNF-α and IgE in the late phase of contact hypersensitivity induced by trimellitic anhydride

Abstract: Trimellitic anhydride (TMA) is widely used industrially to make epoxy and alkyd resins, plasticizers and surfactants. The purpose of this study was to investigate whether contact hypersensitivity (

Cited by 12 publications

References 32 publications

Mast cells play a key role in Th2 cytokine-dependent asthma model through production of adhesion molecules by liberation of TNF-α

Mast cells play a key role in Th2 cytokine-dependent asthma model through production of adhesion molecules by liberation of TNF-α

Involvement of the Cannabinoid CB2 Receptor and Its Endogenous Ligand 2-Arachidonoylglycerol in Oxazolone-Induced Contact Dermatitis in Mice

IgE regulates T helper cell differentiation through FcγRIII mediated dendritic cell cytokine modulation

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