| pubmed-article:7992386 | pubmed:abstractText | Recently, considerable progress has been made in understanding the molecular basis by which cytokines released from CD4+ helper T cells contribute to allergic disease. A subset of CD4+ helper T cells, termed TH2 cells, produce interleukin 4 (IL-4) and IL-5, but not interferon gamma. IL-4 has a critical role in causing B-cell immunoglobulin-isotype switch leading to IgE synthesis, and IL-5 governs eosinophilic inflammation of airway tissue. Studies on the mechanisms whereby TH2 cells, and non-T cells such as metachromatic cells, produce a highly restricted panel of cytokines has revealed molecular mechanisms that may affect our views on the induction and treatment of asthma, and these are discussed in this review by Gary Anderson and Anthony Coyle. TH2 cytokine biology may enable pharmacologists to design better, and perhaps even preventative, therapies for the treatment of asthma and allergy. Surprisingly IL-4, rather than IL-5, is emerging as a critical drug target owing to its central role in the regulation of CD4+ helper T cell phenotype commitment. | lld:pubmed |
