Affiliations 

  • 1 Department of Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia; Department of Pharmacology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia
  • 2 Department of Pharmacology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. Electronic address: norazizan@um.edu.my
  • 3 Jeffrey Cheah School of Medicine, Monash University Malaysia, Jalan Lagoon, 47500 Bandar Sunway, Selangor, Malaysia
  • 4 Department of Pharmacology, Faculty of Medicine, MAHSA University, Bandar Saujana Putra, Selangor, Malaysia
  • 5 Department of Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia
Hum Immunol, 2019 Sep;80(9):755-763.
PMID: 31054782 DOI: 10.1016/j.humimm.2019.04.018

Abstract

Asthma is a complex disorder involving immunologic, environmental, genetic and other factors. Today, asthma is the most common disease encountered in clinical medicine in both children and adults worldwide. Asthma is characterized by increased responsiveness of the tracheobronchial tree resulting in chronic swelling and inflammation of the airways recognized to be controlled by the T-helper 2 (Th2) lymphocytes, which secrete cytokines to increase the production of IgE by B cells. There are many cytokines implicated in the development of the chronic inflammatory processes that are often observed in asthma. Ultimately, these cytokines cause the release of mediators such as histamine and leukotrienes (LT), which in turn promote airway remodeling, bronchial hyperresponsiveness and bronchoconstriction. The CD4+ T-lymphocytes from the airways of asthmatics express a panel of cytokines that represent the Th2 cells. The knowledge derived from numerous experimental and clinical studies have allowed physicians and scientists to understand the normal functions of these cytokines and their roles in the pathogenesis of asthma. The main focus of this review is to accentuate the relationship between various cytokines implicated in human asthma. However, some key findings from animal models will be highlighted to support the discoveries from clinical studies.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.