Exact(7)
Trigeminal fiber collaterals produce a sterile dural inflammation that lead to mast cell degranulation and the trigeminoparasympathetic reflex causes a late and sustained medial meningeal artery dilation (see Fig. S6 in Katata et al. [79] for more details).
Trigeminal fiber collaterals produce a sterile dural inflammation that lead to mast cell degranulation and the trigeminoparasympathetic reflex causes a late and sustained medial meningeal artery dilation (see Fig. S6 in Katata et al. [79]. for more details on their proposed model).
Such exposure presumably would provoke formation of specific IgE antibodies that could bind to mast cells and, upon subsequent exposure, lead to mast cell degranulation and the elaboration of mediators traditionally associated with the asthmatic (early- and late-phase) response.
In physiological conditions, their numbers remain relatively constant; however, proliferation and the enhancement of the mechanisms described above lead to mast cell hyperplasia during hypersensitivity reactions and infections and in response to various disease processes [ 27– 29].
Moreover, the possibility that in the presence of helminth infections, IgE antibodies generated are of lower affinity and therefore can not lead to mast cell degranulation has also been put forward [ 22].
The mannitol challenge is a novel indirect bronchial challenge [ 7, 8], which exerts an osmotic effect on the airway and consequently has the potential to lead to mast cell activation [ 9].
Similar(53)
This mouse strain has an inversion upstream of the Kit gene that leads to mast cell deficiency due to a selective reduction of the Kit expression.
FcεR1γ for example, is expressed on the surface of mast cell and cross-linking of these IgE bound receptors leads to mast cell degranulation, cytokine production, prostaglandin synthesis, survival and passive systemic anaphylaxis [ 49].
Another study also indicated that acute psychological stress could lead to cardiac mast cell degranulation through CRH acting directly or through neurotensin[ 30].
Elevated IgE levels in germ-free mice lead to increased mast-cell-surface-bound IgE and exaggerated oral-induced systemic anaphylaxis.
The Th2 associated cyto- and chemokines IL-4, IL-5, IL-13, TARC/CCL17, and MDC/CCL22, in turn, lead to recruitment of mast cells and eosinophils whose mediator release includes histamine [2, 3].
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