Asthma: mechanisms of disease persistence and progression.
By L. Cohn, J. Elias, G. Chupp. Annual Review of Immunology, 2004
923 citations recorded by the source corpus.
Subfields: Immunology, Physiology, Surgery
View Paper: https://www.semanticscholar.org/paper/f58c0f78d72f7a9aac5449134c754f11dec39e3d
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Citations in the corpus
- Lung natural helper cells are a critical source of Th2 cell-type cytokines in protease allergen-induced airway inflammation. (2012, background): “, 2006), Th2 cells are generally thought to be the critical source of those cytokines (Cohn et al., 2004).”
- The development of allergic inflammation (2008, background): “This may contribute to the development of 'non-specific airway hyperreactivity' to agonists such as histamine, cys-LTs and methacholine, which is a hallmark of asthm”
- The biological functions of T helper 17 cell effector cytokines in inflammation. (2008, positive): “Evidence from clinical observations and from studies on experimental animals supports the idea that uncontrolled Th2 cell responses , as well downstream cytokines IL-4, IL-5, and IL-13, are underlying the development of atopic diseases, such as asthma (Cohn et al., 2004).”
- Cytokine regulation of tight junctions (2008, background): “However, in airway epithelial cells, IFN-γ exposure has anti-inflammatory properties and promotes epithelial barrier function; indicative of pleiotropic effects [13,14].”