Serum levels of soluble stem cell factor and soluble KIT are elevated in patients with atopic dermatitis and correlate with the disease severity

Kanbe, Takayoshi; Soma, Yoshinao; Kawa, Yoko; Kashima, Masato; Mizoguchi, Masahiro

doi:10.1046/j.1365-2133.2001.04224.x

Cited by 31 publications

(34 citation statements)

References 33 publications

(39 reference statements)

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“…The dose dependency of adverse events supports the hypothesis that imatinib-related cutaneous reactions are mediated by changes in tyrosine kinase signaling rather than immunologic mechanisms [40,41]. Mast cells and epidermal melanocytes express c-Kit [42]. While stimulation, rather than inhibition, of c-Kit has been proposed as a causative mechanism in atopic dermatitis [42], the possibility that altered c-Kit affects the development of epidermal inflammation and other changes in epidermal homeostasis merits further investigation.…”

Section: Cutaneous Reactionsmentioning

confidence: 59%

“…Mast cells and epidermal melanocytes express c-Kit [42]. While stimulation, rather than inhibition, of c-Kit has been proposed as a causative mechanism in atopic dermatitis [42], the possibility that altered c-Kit affects the development of epidermal inflammation and other changes in epidermal homeostasis merits further investigation. There is a report of localized depigmentation in a CML 276 patient after 6 months of treatment with imatinib, possibly related to inhibition of the melanocyte c-Kit receptor tyrosine kinase [43]; vitiligo has also been reported.…”

Section: Cutaneous Reactionsmentioning

confidence: 99%

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Indications for Imatinib Mesylate Therapy and Clinical Management

2004

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Imatinib mesylate (Gleevec ® , Glivec ® , formerly STI571; Novartis Pharma AG; Basel, Switzerland) is a rationally-designed, molecularly-specific oral anticancer agent that selectively inhibits several protein tyrosine kinases central to the pathogenesis of human cancer. It has demonstrated remarkable clinical efficacy in patients with chronic myeloid leukemia and malignant gastrointestinal stromal tumors. Treatment with imatinib is generally well tolerated, and the risk for severe adverse effects is low. Adverse effects most commonly include mild-to-moderate edema, nausea and vomiting, diarrhea, muscle cramps, and cutaneous reactions. Hepatic transaminase level elevations and myelosuppression occur less frequently and resolve with interruption of imatinib therapy. In general, the incidence and severity of adverse effects tend to correlate with imatinib dose and, in chronic myeloid leukemia patients, the phase of disease; but, patient age and other factors are also associated with some types of reactions. With prompt and appropriate intervention, adverse effects in imatinib-treated patients have proven to be manageable across the spectrum of severity, and they seldom require permanent cessation of therapy. Dose reduction is not usually necessary, and reduction to subtherapeutic levels is not recommended.

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Section: Cutaneous Reactionsmentioning

confidence: 59%

Section: Cutaneous Reactionsmentioning

confidence: 99%

Indications for Imatinib Mesylate Therapy and Clinical Management

2004

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“…In fact, preincubation with suboptimal and optimal doses of SCF enhanced ␤-hexosaminidase release and intracellular Ca 2ϩ mobilization in response to IgE-specific Ag. Because epithelial cells, in addition to fibroblasts (28), produce SCF at the local site in patients with allergic rhinitis (53) and the serum levels of SCF are enhanced in patients with atopic dermatitis in correlation with the severity of dermatitis (54), local levels of SCF might change in response to the peripheral condition. Thus, SCF may control mast cells functions: particularly motility and degranulation, corresponding to the peripheral levels of SCF.…”

Section: Discussionmentioning

confidence: 99%

Stem Cell Factor Has a Suppressive Activity to IgE-Mediated Chemotaxis of Mast Cells

Sawada

Shimizu

Tamatani

et al. 2005

The Journal of Immunology

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Stem cell factor (SCF), which is well known as a cytokine capable of amplifying development and functions of mast cells, is mainly released from fibroblasts in the peripheral tissue. To investigate whether SCF controlled chemotactic migration of mast cells induced by IgE-specific Ag, murine bone marrow-derived cultured mast cells (BMCMC) and human cord blood-derived cultured mast cells (HuCMC) were preincubated with SCF. Although BMCMC and HuCMC sensitized with IgE directly moved toward specific Ag, preincubation for even 1 h with an optimal dose of SCF suppressed the IgE-mediated chemotactic movement. No or little inhibitory effect of SCF was detected in BMCMC derived from c-kit receptor-defect WBB6F1-W/Wv mice. In contrast, preincubation of BMCMC and HuCMC with SCF enhanced β-hexosaminidase release and Ca2+ mobilization in response to Ag after sensitization with IgE. Using the real-time record of chemotactic migration, BMCMC preincubated with SCF manifested motionless without degranulation. These results suggest that locally produced SCF may have an inhibitory effect on chemotaxis of mast cells, contributing to their accumulation and enhancement of functions at the peripheral site in allergic and nonallergic conditions.

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“…Stem cell factor (SCF), and the interaction of SCF and its receptor, KIT (tyrosine kinase transmembrane receptor) are the key factors that induce mast cell growth, migration and differentiation. Serum levels of soluble SCF and soluble KIT were significantly elevated in AD patients, positively correlated with the disease severity, and decreased after effective treatment with topical corticosteroids (Kanbe et al, 2001). Significantly higher expression of thymic stromal lymphopoietin (TSLP), an IL-7 -like cytokine, by lesional skin can induce DCs to express Th2 cell -polarizing signals in AD.…”

Section: Neurotrophins and Neuropeptidesgrowth Factors And Hormonesmentioning

confidence: 96%