Schraufstatter IU, Khaldoyanidi SK, DiScipio RG. Complement activation in the context of stem cells and tissue repair. World J Stem Cells 2015; 7(8): 1090-1108 [PMID: 26435769 DOI: 10.4252/wjsc.v7.i8.1090]
Corresponding Author of This Article
Ingrid U Schraufstatter, MD, Torrey Pines Institute for Molecular Studies, 3550 General Atomics Court, San Diego, CA 92121, United States. ischraufstatter@tpims.org
Research Domain of This Article
Immunology
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Stem Cells. Sep 26, 2015; 7(8): 1090-1108 Published online Sep 26, 2015. doi: 10.4252/wjsc.v7.i8.1090
Complement activation in the context of stem cells and tissue repair
Ingrid U Schraufstatter, Sophia K Khaldoyanidi, Richard G DiScipio
Ingrid U Schraufstatter, Sophia K Khaldoyanidi, Richard G DiScipio, Torrey Pines Institute for Molecular Studies, San Diego, CA 92121, United States
Ingrid U Schraufstatter, Richard G DiScipio, Sanford Burnham Medical Research Institute, La Jolla, CA 92037, United States
Author contributions: Schraufstatter IU, Khaldoyanidi SK, and DiScipio RG all wrote the manuscript.
Supported by The grants R21 HL094878 and R21AI10950 to IUS and RGD.
Conflict-of-interest statement: None of the authors have any financial interest to declare.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Ingrid U Schraufstatter, MD, Torrey Pines Institute for Molecular Studies, 3550 General Atomics Court, San Diego, CA 92121, United States. ischraufstatter@tpims.org
Telephone: +1-858-5973898 Fax: +1-858-5973898
Received: November 27, 2014 Peer-review started: November 29, 2014 First decision: January 20, 2015 Revised: July 3, 2015 Accepted: July 24, 2015 Article in press: July 27, 2015 Published online: September 26, 2015
Abstract
The complement pathway is best known for its role in immune surveillance and inflammation. However, its ability of opsonizing and removing not only pathogens, but also necrotic and apoptotic cells, is a phylogenetically ancient means of initiating tissue repair. The means and mechanisms of complement-mediated tissue repair are discussed in this review. There is increasing evidence that complement activation contributes to tissue repair at several levels. These range from the chemo-attraction of stem and progenitor cells to areas of complement activation, to increased survival of various cell types in the presence of split products of complement, and to the production of trophic factors by cells activated by the anaphylatoxins C3a and C5a. This repair aspect of complement biology has not found sufficient appreciation until recently. The following will examine this aspect of complement biology with an emphasis on the anaphylatoxins C3a and C5a.
Core tip: This review article provides an overview over the scenarios, where complement activation contributes to tissue repair and regeneration through its effect on stem and progenitor cells, which is an area that needs further investigation.
