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T cell-dependent mast cell degranulation and release of serotonin in murine delayed-type hypersensitivity.

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TLDR
Light microscopic radioautographs from animals treated with [3H]5-HT indicated that local mast cells released 5-HT between 6 and 18 h during the evolution of DTH, which indicated that mast cell degranulation and 5- HT release in murine DTH were probably T cell dependent.
Abstract
We have previously suggested that the release of serotonin (5-hydroxytryptamine) (5-HT) by local tissue mast cells is required for the elicitation of delayed-type hypersensitivity (DTH) in mice. In the current study, light microscopic radioautographs from animals treated with [3H]5-HT indicated that local mast cells released 5-HT between 6 and 18 h during the evolution of DTH. Ultrastructural examination of mast cells revealed surface activation, indicated by extension of surface filopodia, and degranulation by fusion and exocytosis. Light and electron microscopic studies of the endothelium of postcapillary venules at sites of DTH revealed the development of gaps between adjacent cells. The development of gaps permitted extravasation of tracers that was abolished by depletion or antagonism of 5-HT. Thus mast cells degranulated and released 5-HT in DTH, and this 5-HT acted on local vessels. Recipients of nonadherent, non-immunoglobulin-bearing sensitized lymphocytes also demonstrated similar mast cell degranulation and the formation of endothelial gaps. This indicated that mast cell degranulation and 5-HT release in murine DTH were probably T cell dependent.

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Maintenance of serotonin in the intestinal mucosa and ganglia of mice that lack the high-affinity serotonin transporter: Abnormal intestinal motility and the expression of cation transporters.

TL;DR: Stool water and colon motility were increased in most SERT −/− animals; however, the increase in motility occasionally alternated irregularly with decreased motility (constipation), whereas the transient constipation may be caused by episodes of enhanced 5- HT release leading to 5-HT receptor desensitization.
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Effector and regulatory mechanisms in allergic contact dermatitis

TL;DR: ACD should be considered as a breakdown of the skin immune tolerance to haptens, and the nature, the mode and the site of action of the regulatory T cells that control the skin inflammation are addressed with the aim of developing new strategies of tolerance induction in allergic patients.
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Acute stress increases permeability of the blood-brain-barrier through activation of brain mast cells.

TL;DR: It is shown that acute stress by immobilization increased permeability of rat BBB to intravenous 99Technetium gluceptate (99Tc) and induced activation of mast cells in diencephalon, the site where most mast cells are found in the rat brain.
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Mast cells and inflammation.

TL;DR: The role of mast cells in inflammatory reactions of diverse origin, such as delayed type hypersensitivity, atopy, immune complex-mediated inflammation and innate immune responses are focused on.
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Differential release of serotonin and histamine from mast cells

TL;DR: The ability to secrete differentially expands the physiological potential of the mast cell, and suggests that release of serotonin may not always indicate mast cell secretion via exocytosis of secretory granules.
References
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Journal ArticleDOI

STUDIES ON INFLAMMATION: I. The Effect of Histamine and Serotonin on Vascular Permeability: An Electron Microscopic Study

TL;DR: The mechanism, whereby histamine and serotonin increase the permeability of blood vessels, was studied in the rat by means of the electron microscope, and electron microscopic findings suggested that the endothelial cells become partially disconnected along the intercellular junctions.
Journal ArticleDOI

Augmentation of delayed-type hypersensitivity by doses of cyclophosphamide which do not affect antibody responses.

TL;DR: The results suggest that antibody feedback is not the sole regulator of delayed reactions; the possibility that suppressor T cells may also be involved is discussed.
Journal ArticleDOI

Influence of dose and route of antigen injection on the immunological induction of T cells.

TL;DR: DTH fails to reappear in respose to secondary stimulation except in splenectomized mice in whom the development of DTH is not suppressed, even by massive doses of SRBC, and blocking of induction and expression may depend, therefore, on different mechanisms.
Journal ArticleDOI

Differential release of serotonin and histamine from mast cells

TL;DR: The ability to secrete differentially expands the physiological potential of the mast cell, and suggests that release of serotonin may not always indicate mast cell secretion via exocytosis of secretory granules.
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