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Licensed Unlicensed Requires Authentication Published by De Gruyter July 27, 2016

More than just innate affairs – on the role of annexins in adaptive immunity

  • Heiko Weyd EMAIL logo
From the journal Biological Chemistry

Abstract

In more than 30 years of research annexins have been demonstrated to regulate immune responses. The prototype member of this family, annexin (Anx) A1, has been widely recognized as an anti-inflammatory mediator affecting migration and cellular responses of various cell types of the innate immune system. Evidently, effects on innate immune cells also impact on the course of adaptive immune responses. Innate immune cells provide a distinct cytokine milieu during initiation of adaptive immunity which regulates the development of T cell responses. Moreover, innate immune cells such as monocytes can differentiate into dendritic cells and take an active part in T cell stimulation. Accumulating evidence shows a direct role for annexins in adaptive immunity. Anx A1, the annexin protein studied in most detail, has been shown to influence antigen presentation as well as T cells directly. Moreover, immune modulatory roles have been described for several other annexins such as Anx A2, Anx A4, Anx A5 and Anx A13. This review will focus on the involvement of Anx A1 and other annexins in central aspects of adaptive immunity, such as recruitment and activation of antigen presenting cells, T cell differentiation and the anti-inflammatory removal of apoptotic cells.

Acknowledgments

The author would like to thank P.H. Krammer (Division of Immunogenetics (D030) DKFZ, Heidelberg, Germany) for continuous scientific support and critical discussions as well as A. Schmidt (Department in Medicine Solna, Karolinska Institute, Stockholm, Sweden) and G. Hämmerling, A. Kuhn, F. Bujupi, C. Eck and K. Bode (Division of Immunogenetics (D030) DKFZ, Heidelberg, Germany) for critical reading of the manuscript and for helpful discussions.

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Received: 2016-4-27
Accepted: 2016-7-22
Published Online: 2016-7-27
Published in Print: 2016-10-1

©2016 Walter de Gruyter GmbH, Berlin/Boston

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