Butler, C.A., McQuaid, S., Taggart, C.C., Weldon, S., Carter, R., Skibinski, G., Warke, T.J., Choy, D.F., McGarvey, L.P., Bradding, P., Arron, J.R. and Heaney, L.G. (2012) Glucocorticoid receptor β and histone deace tylase 1 and 2 expression in the airways of severe asthma. Thorax, 67, 392-398. Epub 8 December 2011.
has been cited by the following article:
Clinical and pathobiological heterogeneity of asthma—Mechanisms of severe and glucocorticoid-resistant asthma
Asthma Phenotype; Genome-Wide Association Study (GWAS); Glucocorticoid (GC)-Resistant (GC-R) Asthma; Severe Asthma
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.