scholarly journals PGD2 deficiency exacerbates food antigen-induced mast cell hyperplasia

2015 ◽  
Vol 6 (1) ◽  
Author(s):  
Tatsuro Nakamura ◽  
Shingo Maeda ◽  
Kazuhide Horiguchi ◽  
Toko Maehara ◽  
Kosuke Aritake ◽  
...  
2017 ◽  
Vol 139 (3) ◽  
pp. 987-996.e10 ◽  
Author(s):  
Asuka Honjo ◽  
Nobuhiro Nakano ◽  
Susumu Yamazaki ◽  
Mutsuko Hara ◽  
Koichiro Uchida ◽  
...  

2008 ◽  
Vol 31 (3) ◽  
pp. 464-468 ◽  
Author(s):  
Takuya Nagata ◽  
Takeshi Nabe ◽  
Masanori Fujii ◽  
Nobuaki Mizutani ◽  
Shigekatsu Kohno

1977 ◽  
Vol 42 (2) ◽  
pp. 174-178 ◽  
Author(s):  
A. Tucker ◽  
I. F. McMurtry ◽  
A. F. Alexander ◽  
J. T. Reeves ◽  
R. F. Grover

Changes in the density and distribution of pulmonary mast cells were determined in six mammalian species exposed to hypobaric hypoxia (PB = 435 Torr) for 19–48 days. Control animals were studied at 1,600 m (PB = 635 Torr). Total lung mast cell hyperplasia was observed only in calves exposed to high altitude. Pigs, rats, and sheep exhibited small, but insignificant, increases in mast cell density. Perivascular mast cell proliferation adjacent to vessels of 30–500 mum in diameter was seen in both calves and pigs. Bronchial, alveolar septal, and systemic tissue (tongue) mast cell hyperplasia was not observed in any of the species. Three indices of pulmonary hypertension (right ventricular hypertrophy, medial thickness of pulmonary arteries, and pulmonary arterial pressure) correlated with perivascular mast cell density. The findings indicate that perivascular mast cell proliferation may relate more to the morphological pulmonary vascular changes and to pulmonary hypertension than to hypoxia, leading to the speculation that mast cells increase in number in response to the hypertension, rather than to mediate and maintain the hypertension.


1991 ◽  
Vol 96 (2) ◽  
pp. 168-174 ◽  
Author(s):  
Patrick J. Haley ◽  
Mark Schuyler ◽  
Katherine Gott ◽  
Thomas B. Casale

Blood ◽  
2001 ◽  
Vol 98 (3) ◽  
pp. 880-882 ◽  
Author(s):  
Trisha Daley ◽  
Dean D. Metcalfe ◽  
Cem Akin

Abstract Gain-of-function mutations in c-kit, which appear to contribute to mast cell hyperplasia, have been detected in both limited and aggressive forms of mastocytosis, suggesting that other mutations or polymorphisms may contribute to the clinical phenotype. Because addition of interleukin-4 (IL-4) to mast cell cultures is reported to induce apoptosis, the hypothesis was considered that individuals carrying the gain-of-function polymorphism Q576R in the cytoplasmic domain of the α-subunit of the IL-4 receptor (IL-4R) might be relatively resistant to the gain-of-function mutation in c-kit. To assess this possibility, 36 patients with either cutaneous or systemic mastocytosis were studied for association with the Q576R polymorphism. The Q576R polymorphism was found more frequently in those with disease limited to skin and who exhibited lower levels of surrogate disease markers. These data suggest that the Q576R IL-4R α- chain polymorphism may mitigate disease expression and confer a better prognosis in patients with mastocytosis.


2008 ◽  
Vol 60 (10) ◽  
pp. 599-607 ◽  
Author(s):  
Ming-Cai Zhang ◽  
Hiroshi Furukawa ◽  
Kazuhiro Tokunaka ◽  
Kan Saiga ◽  
Fumiko Date ◽  
...  

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