HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lang, R. Articles by Mages, J. Search for Related Content PubMed PubMed Citation Articles by Lang, R. Articles by Mages, J.

DUSP Meet Immunology: Dual Specificity MAPK Phosphatases in Control of the Inflammatory Response¹

Institute of Medical Microbiology, Immunology and Hygiene, Technical University Munich, Immunology and Hygiene, Munich, Germany

The MAPK family members p38, JNK, and ERK are all activated downstream of innate immunity’s TLR to induce the production of cytokines and inflammatory mediators. However, the relative intensity and duration of the activation of different MAPK appears to determine the type of immune response. The mammalian genome encodes a large number of dual specificity phosphatases (DUSP), many of which act as MAPK phosphatases. In this study, we review the emergence of several DUSP as genes that are differentially expressed and regulated in immune cells. Recently, a series of investigations in mice deficient in DUSP1, DUSP2, or DUSP10 revealed specificity in the regulation of the different MAPK proteins, and defined essential roles in models of local and systemic inflammation. The DUSP family is proposed as a set of molecular control devices specifying and modulating MAPK signaling, which may be targeted to unleash or attenuate innate and adaptive immune effector functions.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ The work performed in the Lang laboratory was supported by the Deutsche Forschungsgemeinschaft (SFB 576, TP 11 and Grant LA 1262/4-1) and the Bundesministerium für Bildung und Forschung (NGFN-2 Grant 01GS0402).

² Address correspondence and reprint requests to Dr. Roland Lang, Institute of Medical Microbiology, Immunology and Hygiene, Technical University Munich, Immunology and Hygiene, Trogerstrasse 30, Munich 81675, Germany. E-mail address: Roland.Lang{at}lrz.tum.de

³ Abbreviations used in this paper: DC, dendritic cell; MKP, MAPK phosphatase; DUSP, dual specificity phosphatases; MKB, MAPK binding domain; LCMV, lymphocytic choriomeningitis virus.

This article has been cited by other articles:

				J. R. Cerhan, S. M. Ansell, Z. S. Fredericksen, N. E. Kay, M. Liebow, T. G. Call, A. Dogan, J. M. Cunningham, A. H. Wang, W. Liu-Mares, et al. Genetic variation in 1253 immune and inflammation genes and risk of non-Hodgkin lymphoma Blood, December 15, 2007; 110(13): 4455 - 4463. [Abstract] [Full Text] [PDF]

				D. M. Cooper, S. Radom-Aizik, C. Schwindt, and F. Zaldivar Jr. Dangerous exercise: lessons learned from dysregulated inflammatory responses to physical activity J Appl Physiol, August 1, 2007; 103(2): 700 - 709. [Abstract] [Full Text] [PDF]