Article citationsMore>>
Wakashin, H., Hirose, K., Maezawa, Y., Kagami, S., Suto, A., Watanabe, N., Saito, Y., Hatano, M., Tokuhisa, T., Iwakura, Y., Puccetti, P., Iwamoto, I. and Nakajima, H. (2008) IL-23 and Th17 cells enhance Th2-cell-mediated eosinophilic airway inflammation in mice. American Journal of Respiratory and Critical Care Medicine, 178, 1023-1032. Epub 11 September 2008.
doi:10.1164/rccm.200801-086OC
has been cited by the following article:
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TITLE:
Clinical and pathobiological heterogeneity of asthma—Mechanisms of severe and glucocorticoid-resistant asthma
AUTHORS:
Yasuhiro Matsumura
KEYWORDS:
Asthma Phenotype; Genome-Wide Association Study (GWAS); Glucocorticoid (GC)-Resistant (GC-R) Asthma; Severe Asthma
JOURNAL NAME:
Health,
Vol.5 No.2A,
February
27,
2013
ABSTRACT:
It
is increasingly recognized that asthma represents
a syndrome, and there is clinical and pathobiological heterogeneity. Many genes
are reported to be associated with asthma, and may be involved in the disease
heterogeneity. Diverse cells, such as T helper 1 (Th1)-cells, Th2-cells,
Th17-cells, airway epithelial cells, and innate and adaptive immunity
associated cells, contribute to the pathobiology of asthma independently of
each other or they can also coexist and interact. Although, generally, Th2
immunity is important in most asthma endotypes, non- Th2-driven inflammation
tends to be difficult to manage. Recently, increased attention has been focused
on severe asthma and glucocorticoid (GC)-resistant (GC-R) asthma, in which
diverse inflammatory processes may be involved. Treatment approaches should
take into account pathological differences.
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