The role of the T cell in asthma Douglas S. Robinson, MD, FRCP  Journal of Allergy and Clinical Immunology  Volume 126, Issue 6, Pages 1081-1091 (December 2010) DOI: 10.1016/j.jaci.2010.06.025 Copyright © 2010 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 1 Immunologic interactions of T cells in patients with asthma. Activation of airway epithelium (Epi) by allergens and viruses through Toll-like receptors (TLR) and damage receptors (DAMPs) leads to release of the pro-TH2 cytokines IL-25, IL-33, and TSLP, which act through dendritic cells (DC), which present allergen peptides through the MHC/T-cell receptor (TCR) complex, and directly on T cells and non-T cells to favor TH2 cytokine production (IL-4, IL-5, IL-6, IL-9, IL-13, and possibly IL-31). Some of these cytokines act on (and are produced by) eosinophils (Eo), which might act in asthma exacerbations, and basophils (Ba) and mast cells (MC), and IL-4 and IL-13 switch B cells to IgE production. TH2 cytokines also act on structural cells, such as epithelium, to increase mucus production, and MC interaction with airway smooth muscle (ASM) might induce AHR. NKT cells, γδ T cells (both activated through T-cell receptor and CD1), and CD8+ T cells can also produce TH2 cytokines but might also suppress TH2 responses in certain settings. Treg cells, including FoxP3+CD25+ and IL-10–producing Treg cells, have the potential to suppress TH2 cells. Journal of Allergy and Clinical Immunology 2010 126, 1081-1091DOI: (10.1016/j.jaci.2010.06.025) Copyright © 2010 American Academy of Allergy, Asthma & Immunology Terms and Conditions