In allergic diseases such as asthma, hay fever, and rhinitis an allergen stimulates the release of antibodies that attach themselves to mast cells causing these cells to release histamine, which can cause symptoms like itching of the nose, skin and eyes, sneezing, and wheezing. The characteristic "Th2 immune response" observed in allergy sufferers is an acquired immune response whose most prominent feature is high antibody production relative to the amount of cytotoxic T cells. Classical antihistamine drugs bind to but do not activate the histamine 1 receptor (H1R), subsequently blocking the allergic response. Interestingly, a recent study in Nature reported that mice deficient in H1Rs were still able to mount a Th2 immune response. In an effort to clarify this discrepancy, Paul Bryce and colleagues from Northwestern University, Chicago, examined H1R-/- mice with asthma and in their study appearing online on May 4 in advance of print publication in the June issue of the Journal of Clinical Investigation, these authors report a previously unknown role for H1R in the development of inflammatory airway responses. They found that these mice do indeed possess a dominant Th2 immune response to allergic antigens, yet they do not develop airway inflammation. Bryce et al. show that this is because the T cells in these mice are not able to travel to the site of allergen exposure - the lung. Histamine was found to act as an attractant for T cells and with no H1Rs present for histamine to bind to, the T cells were not recruited to the lung or able to cause the characteristic inflammatory allergic response in these mice. This advancement of our understanding of the roles of histamine in allergic disease indicates that blocking H1R with currently available drugs might have potential benefit for patients.
TITLE: The H1 histamine receptor regulates allergic lung responses
Paul J. Bryce
Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.
Phone: (312) 503-0077; Fax: (312) 503-0078; E-mail: email@example.com.
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