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Eur Respir J 2005; 26:918-932
Copyright ©ERS Journals Ltd 2005

Regulatory T-lymphocytes in asthma

A. J. M. van Oosterhout1 and N. Bloksma2

1 Laboratory of Allergology and Pulmonary Diseases, Dept Pathology and Laboratory Medicine, University Medical Center Groningen, Groningen University, Groningen, and 2 Faculty of Biology, Utrecht University, Utrecht, The Netherlands.

CORRESPONDENCE: A. J. M. van Oosterhout, Laboratory of Allergology and Pulmonary Diseases and Dept of Pathology and Laboratory Medicine, UMCG, P.O. Box 30.001, 9700 RB, Groningen, The Netherlands. Fax: 31 503121576. E-mail: a.j.m.van.oosterhout{at}path.umcg.nl

Keywords: Allergy, asthma, hygiene, immunotherapy, regulatory T-cell, T-helper cell type 2

Received: February 1, 2005
Accepted June 10, 2005

T-helper cell type (Th)2 lymphocytes play an important role in the initiation, progression and persistence of allergic diseases, including asthma. However, little is known about immunoregulatory mechanisms that determine susceptibility to, severity of, or persistence of asthma. The concept of a disturbed Th1/Th2 balance, although having furthered the present understanding of immunoregulation in asthma, has recently been named a "procrustean paradigm", because of its failure to adequately explain many (pre)clinical observations.

In recent years, the general knowledge regarding the regulation of infectious, autoimmune diseases, asthma and allergen immunotherapy by T-regulatory (Treg) cells, has rapidly increased. Many different Treg subsets have been described, including CD8+ Treg cells, natural killer (NK) cells and several different CD4+ Treg cell subsets.

In this review, the authors will focus on two major and well-described CD4+ Treg cell subsets. These consist of naturally occurring CD25+ Treg cells and adaptive Treg cells that are postulated to prevent immune responses against self-antigens and adaptive immune responses, respectively.

The adaptive T-regulatory cells are further subdivided into T-regulatory cells type 1 and T-helper cell type 3 that mediate suppression exclusively via the cytokines interleukin-10 and transforming growth factor-ß, respectively.




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