Pathophysiology of human basophils and mast cells in allergic disorders

Marone, Gianni; Casolaro, Vincenzo; Cirillo, R; Stellato, Cristiana; Genovese, Arturo

doi:10.1016/0090-1229(89)90111-6

Cited by 53 publications

(24 citation statements)

References 132 publications

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“…2a). Upon IgE-mediated activation of human lung mast cells, only a small portion (Ͻ5%) of cellular arachidonic acid was reportedly released and converted mainly to PGD 2 and LTC 4 in approximately equal amounts (0.15 nmol/10 6 cells) (21,30,31). Human skin mast cells produce PGD 2 in amounts similar to lung mast cells, but reportedly generate very little LTC 4 (32).…”

Section: Discussionmentioning

confidence: 99%

A Comparison of Mediators Released or Generated by IFN-γ-Treated Human Mast Cells Following Aggregation of FcγRI or FcεRI

Okayama

Hagaman

Metcalfe

2001

The Journal of Immunology

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The high affinity receptor for IgG (FcγRI, CD64) is expressed on human mast cells, where it is up-regulated by IFN-γ and, thus, may allow mast cells to be recruited through IgG-dependent mechanisms in IFN-γ-rich tissue inflammation. However, the mediators produced by human mast cells after aggregation of FcγRI are incompletely described, and it is unknown whether these mediators are distinct from those produced after activation of human mast cells via FcεRI. Thus, we investigated the release of histamine and arachidonic acid metabolites and examined the chemokine and cytokine mRNA profiles of IFN-γ-treated cultured human mast cells after FcγRI or FcεRI aggregation. Aggregation of FcγRI resulted in histamine release and PGD2 and LTC4 generation. These responses were qualitatively indistinguishable from responses stimulated via FcεRI. Aggregation of FcεRI or FcγRI led to an induction or accumulation of 22 cytokine and chemokine mRNAs. Among them, seven cytokines (TNF-α, IL-1β, IL-5, IL-6, IL-13, IL-1R antagonist, and GM-CSF) were significantly up-regulated via aggregation of FcγRI compared with FcεRI. TNF-α mRNA data were confirmed by quantitative RT-PCR and ELISA. Furthermore, we confirmed histamine and TNF-α data using IFN-γ-treated purified human lung mast cells. Thus, aggregation of FcγRI on mast cells led to up-regulation and/or release of three important classes of mediators: biogenic amines, lipid mediators, and cytokines. Some cytokines, such as TNF-α, were released and generated to a greater degree after FcγRI aggregation, suggesting that selected biologic responses of mast cells may be preferentially generated through FcγRI in an IFN-γ-rich environment.

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Section: Discussionmentioning

confidence: 99%

A Comparison of Mediators Released or Generated by IFN-γ-Treated Human Mast Cells Following Aggregation of FcγRI or FcεRI

Okayama

Hagaman

Metcalfe

2001

The Journal of Immunology

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“…It is known that, in D. pt-allcrgic patients, addition of crude extracts of D. pt or purified Derp I allergen can in duce activation of FceRI-bcaring mast cells or basophils, generating release of histamine [44], In the same manner, platelets from patients sensitive to D. pt are susceptible to be activated by the specific allergen, through IgE recep tors of low affinity present on their surfaces [24,25,34[. Though the participation of platelets in allergic diseases is still debated [45], the model of platelet activation could be useful for the evaluation of the IgE-dcpendent biological activities of other Derp 1-derivcd peptides.…”

Section: Discussionmentioning

confidence: 99%

Specific Activation of Platelets from Patients Allergic to <i>Dermatophagoides pteronyssinus</i> by Synthetic Peptides Derived from the Allergen <i>Der p</i> I

Cardot

Pestel

Callebaut

et al. 1992

Int Arch Allergy Immunol

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Previous studies have shown that FcεRII-bearing platelets from patients with allergic disorders could be stimulated either by anti-human IgE antibodies or the relevant allergens to generate cytotoxic mediators. In this report, the reactivity of platelets from Dermatophagoides pteronyssinus (D. pt) -sensitive patients to three Der p I-derived synthetic peptides (52–71,117–133 and 188–199) was investigated. The platelet stimulation observed in D. pt-sensitive patients was demonstrated to be allergen-specific and to be mediated by IgE. These Der p I-derived peptides failed to stimulate platelets from healthy donors or platelets from non-D. pt-allergic patients. D. pt-sensitive patients responded more frequently to the peptides 52–71 and 117–133 than to the peptide 188–199. Thus, in this model, synthetic peptides selected for their assumed accessibility on the native antigen could be associated to an IgE-dependent biological activity.

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“…Further, it has been demonstrated, in a variety of experimental systems, that autocoids and proteases produced by mast cells (5,6) have the capacity to increase bronchial reactivity; these include platelet activating factor (PAF)' (7), leukotriene E4 (LTE4) (8,9), thromboxane A2 (TxA2) ( 10, 1), prostaglandin F2, (PGF2,) ( 12), and tryptase ( 13). Because the administration of mast cell products can transiently influence airway responsiveness, it has been proposed that mast cell activation may importantly contribute to the bronchial hyperreactivity observed in asthmatic subjects (14)(15)(16). On the other hand, the molecules that have been implicated as potential inducers ofairway hyperreactivity can also be produced by other cell types (15)(16)(17)(18)(19).…”

Section: Introductionmentioning

confidence: 99%

Mast cell activation enhances airway responsiveness to methacholine in the mouse.

Martin

Takeishi²,

Katz³

et al. 1993

J. Clin. Invest.

115

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Pathophysiology of human basophils and mast cells in allergic disorders

Cited by 53 publications

References 132 publications

A Comparison of Mediators Released or Generated by IFN-γ-Treated Human Mast Cells Following Aggregation of FcγRI or FcεRI

A Comparison of Mediators Released or Generated by IFN-γ-Treated Human Mast Cells Following Aggregation of FcγRI or FcεRI

Specific Activation of Platelets from Patients Allergic to <i>Dermatophagoides pteronyssinus</i> by Synthetic Peptides Derived from the Allergen <i>Der p</i> I

Mast cell activation enhances airway responsiveness to methacholine in the mouse.

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