Severe asthma represents a distinct poorly-understood phenotype of asthma that has higher morbidity mortality and a disproportionate need for health care support. Studies have indicated the presence of a specific inflammatory response in severe asthmatics including the paucity of expression of classical Th-2 type cytokines. Following antigenic stimulation naive CD4+ T cells proliferate and differentiate into various effector subsets such as Th-1 and Th-2 cells. A third subset of CD4+ T cells has recently been identified and designated as Th-17 cells which produce IL-17A and F IL-6 and TNF-alpha. In severe asthma there may be a predominant Th-17 phenotype. These cells may promote the release of neutrophil chemotactic factors and induce the expression of GR-beta which is responsible for corticosteroid hyporesponsiveness in immune and structural cells. If the role of Th-17 cytokines is confirmed it might provide a new option in controlling this refractory subtype of asthma.
Piracy-free
Assured Quality
Secure Transactions
Delivery Options
Please enter pincode to check delivery time.
*COD & Shipping Charges may apply on certain items.