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Complement decay accelerating factor (DAF)/CD55 in cancer

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Abstract

The complement system is a powerful innate mechanism involved in protection of the host against pathogens. It also has a role in the clearance of apoptotic cells and has been implicated in a range of pathologies including autoimmunity and graft rejection. The control of complement is mediated through the complement regulatory proteins (CRPs). These are present on most cells and protect normal cells from complement-mediated attack during innate activation. However, in a range of pathologies and cancer, these molecules are up or down regulated, sometimes secreted and even lost. We will review the expression of CRPs in cancer, focussing on CD55 and highlight other roles of the CRPs and their involvement in leukocyte function. We will also provide some data providing a potential mechanism by which soluble CD55 can inhibit T-cell function and discuss some of the implications of this data.

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Authors and Affiliations

  1. CR UK Academic Department of Clinical Oncology, Institute of Infections Immunity and Inflammation, The University of Nottingham, NG5 1PB, Nottingham, UK

    Ian Spendlove, Judith M. Ramage, Richard Bradley & Lindy G. Durrant

  2. Department of Medical Biochemistry and Immunology, University of Wales College of Medicine, Heath Park, CF14 4XN, Cardiff, UK

    Claire Harris

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  1. Ian Spendlove
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  2. Judith M. Ramage
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  3. Richard Bradley
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  4. Claire Harris
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  5. Lindy G. Durrant
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Correspondence to Ian Spendlove.

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This article is a symposium paper from the “Robert Baldwin Symposium: 50 years of Cancer Immunotherapy”, held in Nottingham, Great Britain, on 30 June 2005.

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Spendlove, I., Ramage, J.M., Bradley, R. et al. Complement decay accelerating factor (DAF)/CD55 in cancer. Cancer Immunol Immunother 55, 987–995 (2006). https://doi.org/10.1007/s00262-006-0136-8

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