Skin mast cell histamine release following stem cell factor and high-affinity immunoglobulin E receptor cross-linking in dogs with atopic dermatitis

2001 ◽  
Vol 12 (6) ◽  
pp. 339-346 ◽  
Author(s):  
Bruce Hammerberg ◽  
Thierry Olivry ◽  
Susan M. Orton
Keyword(s):  
Atopic Dermatitis ◽  
Mast Cell ◽  
Stem Cell ◽  
Histamine Release ◽  
Stem Cell Factor ◽  
Immunoglobulin E ◽  
Cross Linking ◽  
High Affinity ◽  
Skin Mast Cell

Pharmacological Study of Stem-Cell-Factor-Induced Mast Cell Histamine Release with Kinase Inhibitors

1995 ◽  
Vol 208 (2) ◽  
pp. 576-581 ◽  
Author(s):  
S. Nagai ◽  
S. Kitani ◽  
K. Hirai ◽  
T. Takaishi ◽  
K. Nakajima ◽  
...  
Keyword(s):  
Mast Cell ◽  
Stem Cell ◽  
Histamine Release ◽  
Stem Cell Factor ◽  
Kinase Inhibitors ◽  
Pharmacological Study

scholarly journals The Mast Cell–SCF–CB1 Interaction Is a Key Player in Seborrheic Keratosis

2020 ◽  
Vol 68 (7) ◽  
pp. 461-471
Author(s):  
Mika Yamanaka-Takaichi ◽  
Koji Sugawara ◽  
Rieko Sumitomo ◽  
Daisuke Tsuruta
Keyword(s):  
Atopic Dermatitis ◽  
Mast Cell ◽  
Stem Cell ◽  
Stem Cell Factor ◽  
Skin Diseases ◽  
Cannabinoid Receptor ◽  
Seborrheic Keratosis ◽  
Novel Treatment ◽  
Important Player

Mast cell (MC) is an important player in the development of skin diseases, including atopic dermatitis, psoriasis, and urticaria. It is reported that MC infiltration and activation are observed around various types of tumors and speculated that MCs play key roles in their pathogenesis. As MCs in human seborrheic keratosis (SK) have not been well investigated, here we focused on the MCs in SK. The number of c-Kit and tryptase-positive MCs was significantly increased around the SK compared with the marginal lesion. Degranulated MCs were also increased around the tumors. Furthermore, MC growth factor, stem cell factor (SCF), expression within the SK was significantly upregulated compared with the marginal lesion. Interestingly, one of the cognitive regulators of SCF expression, cannabinoid receptor type 1 (CB1) immunoreactivity was downregulated within the SK. Our results suggest that MCs play important roles in the pathogenesis of SK and that SCF can be also deeply involved in the development of SKs. Our current results highlight the CB1–SCF–MC interaction as a novel mechanism of SK development and this also will be utilized for developing a novel treatment.

scholarly journals Leukocyte common antigen (CD45) is required for immunoglobulin E-mediated degranulation of mast cells.

1994 ◽  
Vol 180 (2) ◽  
pp. 471-476 ◽  
Author(s):  
S A Berger ◽  
T W Mak ◽  
C J Paige
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Immunoglobulin E ◽  
Tyrosine Phosphatase ◽  
Cross Linking ◽  
Ionophore A23187 ◽  
Wild Type ◽  
Ige Receptor ◽  
High Affinity ◽  
Deficient Mice

We demonstrate using primary mast cell cultures derived from wild-type and CD45-deficient mice that mast cell triggering through the high-affinity immunoglobulin E (IgE) receptor requires the cell surface tyrosine phosphatase CD45. Unlike wild-type cells, cross-linking of surface-bound IgE in mast cells deficient in CD45 does not induce degranulation. Degranulation in these mutant cells does occur after treatment with the calcium ionophore A23187 indicating that the degranulation machinery is intact in these cells. We also demonstrate that the tyrosine phosphatase inhibitors orthoVanadate and perVanadate inhibit degranulation in wild-type mast cells, as does cross-linking of CD45 by anti-CD45 antibodies. Finally, we show that CD45-deficient mice are resistant to IgE-dependent systemic anaphylaxis. These results show that, like the T cell receptor and the antigen receptor on B cells, there is an absolute requirement for CD45 in signaling via the high affinity IgE receptor, expanding the number of receptors for which CD45 is an essential component.

scholarly journals The role of stem cell factor (c-kit ligand) and inflammatory cytokines in pulmonary mast cell activation

Blood ◽  
1996 ◽  
Vol 87 (6) ◽  
pp. 2262-2268 ◽  
Author(s):  
NW Lukacs ◽  
SL Kunkel ◽  
RM Strieter ◽  
HL Evanoff ◽  
RG Kunkel ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mast Cell ◽  
Stem Cell ◽  
Mast Cells ◽  
Histamine Release ◽  
Cell Lines ◽  
Stem Cell Factor ◽  
Upper Airway ◽  
The Other ◽  
Factor C

Mast cells play a critical role in allergic airway responses via IgE- specific activation and release of potent inflammatory mediators. In the present study, we have isolated and characterized primary mast cell lines derived from the upper airways of normal mice. The primary mast cell lines were grown and maintained by incubation with interleukin-3 (IL-3) and stem cell factor (SCF) and shown to be c-kit (SCF receptor) positive by flow cytometry. Subsequently, we examined the proliferation of both airway and bone marrow derived mast cell lines in response to inflammatory and hematopoietic cytokines, including SCF, IL-1, IL-3, interferon-gamma, IL-4, and IL-10. The results from the pulmonary mast cell lines were compared with those from bone marrow derived mast cells. Pulmonary mast cell lines were capable of proliferating in response to IL-3, IL-4, IL-10, and SCF, whereas the combination of SCF with the other cytokines did not increase the response over SCF alone. In contrast, the bone marrow-derived mast cells proliferated strongest to SCF or IL-3, but only modestly to IL-4 and IL-10. Furthermore, the combination of SCF with IL-3, but not the other cytokines, exhibited an increase in bone marrow-derived mast cell proliferation. Cytokine- specific stimulation of histamine release in the airway-derived and bone marrow-derived mast cells showed parallel results. SCF was the only cytokine shown to induce substantial histamine release. However, when certain nonhistamine releasing cytokines were combined with SCF, a synergistic increase in histamine release was induced in upper airway, but not bone marrow-derived mast cells. The results of these studies suggest that cytokines differentially modulate induction of proliferation and degranulation of bone marrow and upper airway-derived mast cells and may further indicate a cytokine activational cascade in tissue mast cells.

Membrane-bound stem cell factor is the major but not only driver of fibroblast-induced murine skin mast cell differentiation

2017 ◽  
Vol 26 (3) ◽  
pp. 255-262 ◽  
Author(s):  
Mandy Leist ◽  
Cathleen Annett Sünder ◽  
Sebastian Drube ◽  
Carolin Zimmermann ◽  
Astrid Geldmacher ◽  
...  
Keyword(s):  
Mast Cell ◽  
Stem Cell ◽  
Cell Differentiation ◽  
Stem Cell Factor ◽  
Skin Mast Cell ◽  
Membrane Bound

scholarly journals SHP2 Phosphatase Promotes Mast Cell Chemotaxis toward Stem Cell Factor via Enhancing Activation of the Lyn/Vav/Rac Signaling Axis

2014 ◽  
Vol 192 (10) ◽  
pp. 4859-4866 ◽  
Author(s):  
Namit Sharma ◽  
Stephanie Everingham ◽  
Baskar Ramdas ◽  
Reuben Kapur ◽  
Andrew W. B. Craig
Keyword(s):  
Mast Cell ◽  
Stem Cell ◽  
Stem Cell Factor ◽  
Signaling Axis ◽  
Cell Chemotaxis

Immunologic mast cell-mediated responses and histamine release are attenuated by heparin

1992 ◽  
Vol 73 (3) ◽  
pp. 1093-1101 ◽  
Author(s):  
J. Lucio ◽  
J. D'Brot ◽  
C. B. Guo ◽  
W. M. Abraham ◽  
L. M. Lichtenstein ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Histamine Release ◽  
Immunoglobulin E ◽  
Specific Antigen ◽  
Calcium Ionophore ◽  
Intradermal Injection ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Dependent Manner

Heparin has been shown to act as a competitive inhibitor of inositol 1,4,5-triphosphate (InsP3) receptors in various cell types. Because InsP3 is one of the second messengers involved in stimulus-secretion coupling in mast cells, it is possible that heparin may inhibit mast cell-mediated reactions. Therefore, in allergic sheep, we tested this hypothesis in two mast cell-mediated reactions induced by immunologic and nonimmunologic stimuli: immediate cutaneous reaction (ICR) and acute bronchoconstrictor response (ABR). In 12 sheep allergic to Ascaris suum antigen, the surface area of the skin wheal was determined 20 min after intradermal injection (0.05 ml) of increasing concentrations of specific antigen, compound 48/80, and histamine, without and after pretreatment with heparin (100, 300, or 1,000 U/kg i.v.). Antigen, compound 48/80, and histamine produced concentration-dependent increases in ICR. Heparin “partially” inhibited the ICR to antigen and compound 48/80 in a dose-dependent manner without modifying the ICR to histamine. The heparin preservative benzyl alcohol was ineffective. In 11 additional sheep, specific lung resistance was measured before and after inhalation challenges with antigen, compound 48/80, and histamine without and with aerosol heparin pretreatment (1,000 U/kg). Heparin blocked the antigen- and compound 48/80-induced bronchoconstriction without modifying the airway effects of histamine. In isolated human uterine mast cells, heparin inhibited the anti-immunoglobulin E- but not the calcium ionophore- (A23187) induced histamine release. These data suggest that heparin inhibits the ICR and ABR induced by stimuli that produce immunologic and nonimmunologic mast cell degranulation without attenuating the effects of histamine.(ABSTRACT TRUNCATED AT 250 WORDS)

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