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Local class switching in nonallergic rhinitis

Payne, Spencer Ca,b; Chen, Philip Ga; Borish, Larryb

Current Opinion in Otolaryngology & Head and Neck Surgery: June 2011 - Volume 19 - Issue 3 - p 193–198
doi: 10.1097/MOO.0b013e328345005c
Allergy: Edited by Berrylin Ferguson

Purpose of review Patients with seasonal and/or persistent symptoms consistent with rhinitis but negative systemic testing for atopy can be diagnostically challenging. It has been postulated that such idiopathic or nonallergic rhinitis may be due to localized class switching and production of IgE in the nasal mucosa, a process which has been termed entopy by some authors. This review analyzes the available data to describe the current understanding of this process as it relates to nonallergic rhinitis.

Recent findings Recent findings have demonstrated local IgE production in the nasal mucosa of patients who are otherwise negative on skin prick, intradermal, or serum testing for atopy. Comparable studies on nonatopic asthmatics have demonstrated evidence of local IgE class switching in lung respiratory mucosa. However, local class switching has only been unambiguously demonstrated in rhinitis patients when atopy is otherwise confirmed by routine testing.

Summary There is significant evidence to indicate that local class switching in nonallergic rhinitis is possible; however, this has not been definitively proven. The question is raised as to whether local class switching can be demonstrated in nonallergic rhinitis and whether that class switching can be determined to be a specific affinity matured response. If present, a local IgE-mediated process is likely to define a cohort of nonallergic rhinitis more likely to respond to allergy-targeted therapies.

aDepartment of Otolaryngology – Head and Neck Surgery, USA

bDivision of Allergy and Clinical Immunology, Department of Medicine, University of Virginia Health System, Charlottesville, Virginia, USA

Correspondence to Spencer C. Payne, MD, P.O. Box 800713, Charlottesville, VA 22908-0713, USA Tel: +1 434 924 5934; fax: +1 434 982 3965; e-mail:

© 2011 Lippincott Williams & Wilkins, Inc.