Hamid, Q.A., Wenzel, S.E., Hauk, P.J., Tsicopoulos, A., Wallaert, B., Lafitte, J.J., Chrousos, G.P., Szefler, S.J. and Leung, D.Y. (1999) Increased glucocorticoid receptor beta in airway cells of glucocorticoid-insensitive asthma. American Journal of Respiratory and Critical Care Medicine, 159, 1600-1604.

has been cited by the following article:

• 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.