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Protective Molecules–C-Reactive Protein (CRP), Serum Amyloid P (SAP), Pentraxin3 (PTX3), Mannose-Binding Lectin (MBL), and Apolipoprotein A1 (Apo A1), and Their Autoantibodies: Prevalence and Clinical Significance in Autoimmunity

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Abstract

Apoptotic defects and impaired clearance of cellular debris are considered key events in the development of autoimmunity, as they can contribute to autoantigen overload, and may initiate an autoimmune response. The pentraxins are a group of highly conserved proteins including the short pentraxins, C-reactive protein (CRP) and serum amyloid-P (SAP), and the long pentraxin-3 (PTX3), which are all involved in innate immunity and in acute-phase responses. Mannan-binding lectin (MBL) is an activator of the complement system, and Apolipoprotein A-1 (Apo A-1) is pivotal in the cholesterol homeostasis and has anti-inflammatory properties. In addition to their role in innate immunity and inflammation, each of these five proteins participates in the removal of damaged and apoptotic cells. In this review, we discuss the clinical significance of different levels of these proteins, their role in the induction or protection from autoimmunity, and the presence of specific autoantibodies against them in the different autoimmune diseases.

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  1. Center for Autoimmune Diseases and Department of Medicine B, Chaim Sheba Medical Center Tel-Hashomer, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel

    Martine Szyper Kravitz, Milena Pitashny & Yehuda Shoenfeld

  2. Incumbent of the Laura Schwatz-Kipp chair for autoimmunity, TelAviv University, Tel Aviv, Israel

    Yehuda Shoenfeld

  3. Department of Medicine B, Chaim Sheba Medical Center, Tel-Hashomer, Israel, 52621

    Yehuda Shoenfeld

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Kravitz, M.S., Pitashny, M. & Shoenfeld, Y. Protective Molecules–C-Reactive Protein (CRP), Serum Amyloid P (SAP), Pentraxin3 (PTX3), Mannose-Binding Lectin (MBL), and Apolipoprotein A1 (Apo A1), and Their Autoantibodies: Prevalence and Clinical Significance in Autoimmunity. J Clin Immunol 25, 582–591 (2005). https://doi.org/10.1007/s10875-005-7828-2

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  • DOI: https://doi.org/10.1007/s10875-005-7828-2

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