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  • 1
    Abstract: Mast cell-deficient Kit(W-sh) "sash" mice are widely used to investigate mast cell functions. However, mutations of c-Kit also affect additional cells of hematopoietic and nonimmune origin. In this study, we demonstrate that Kit(W-sh) causes aberrant extramedullary myelopoiesis characterized by the expansion of immature lineage-negative cells, common myeloid progenitors, and granulocyte/macrophage progenitors in the spleen. A consistent feature shared by these cell types is the reduced expression of c-Kit. Populations expressing intermediate and high levels of Ly6G, a component of the myeloid differentiation Ag Gr-1, are also highly expanded in the spleen of sash mice. These cells are able to suppress T cell responses in vitro and phenotypically and functionally resemble myeloid-derived suppressor cells (MDSC). MDSC typically accumulate in tumor-bearing hosts and are able to dampen immune responses. Consequently, transfer of MDSC from naive sash mice into line 1 alveolar cell carcinoma tumor-bearing wild-type littermates leads to enhanced tumor progression. However, although it can also be observed in sash mice, accelerated growth of transplanted line 1 alveolar cell carcinoma tumors is a mast cell-independent phenomenon. Thus, the Kit(W-sh) mutation broadly affects key steps in myelopoiesis that may have an impact on mast cell research.
    Type of Publication: Journal article published
    PubMed ID: 23636054
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  • 2
    Electronic Resource
    Electronic Resource
    ISSN: 1434-4726
    Keywords: Key words Familial idiopathic facial palsy ; Human leukocyte antigen
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The etiology of idiopathic facial palsy (IFP) is still not defined. Familial inheritance has been found in 4–14% of cases. Among 116 patients with IFP admitted to the otolaryngology and neurology clinics at Kütahya State Hospital, 12 had positive family histories involving 10 different families. Review of the patients’ histories showed that 13 members of families previously had IFP. In all, the 25 patients with familial IFP consisted of 12 males and ¶13 females and had an average age at onset of 34.3 years. Class I human leukocyte antigen (HLA) was investigated in 11 patients with familial IFP belonging to four separate families. The follow-up period was approximately 2 months. All cases except one recovered completely, with the latter patient having minimal contracture and facial paresis. However, HLA showed no significant increases in class I antigens. No notable difference was found in the clinical courses of patients with familial and non-familial IFP.
    Type of Medium: Electronic Resource
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