scholarly journals Monocytes and macrophages in tissue repair: Implications for immunoregenerative biomaterial design

2016 ◽  
Vol 241 (10) ◽  
pp. 1084-1097 ◽  
Author(s):  
Molly E Ogle ◽  
Claire E Segar ◽  
Sraeyes Sridhar ◽  
Edward A Botchwey

Monocytes and macrophages play a critical role in tissue development, homeostasis, and injury repair. These innate immune cells participate in guiding vascular remodeling, stimulation of local stem and progenitor cells, and structural repair of tissues such as muscle and bone. Therefore, there is a great interest in harnessing this powerful endogenous cell source for therapeutic regeneration through immunoregenerative biomaterial engineering. These materials seek to harness specific subpopulations of monocytes/macrophages to promote repair by influencing their recruitment, positioning, differentiation, and function within a damaged tissue. Monocyte and macrophage phenotypes span a continuum of inflammatory (M1) to anti-inflammatory or pro-regenerative cells (M2), and their heterogeneous functions are highly dependent on microenvironmental cues within the injury niche. Increasing evidence suggests that division of labor among subpopulations of monocytes and macrophages could allow for harnessing regenerative functions over inflammatory functions of myeloid cells; however, the complex balance between necessary functions of inflammatory versus regenerative myeloid cells remains to be fully elucidated. Historically, biomaterial-based therapies for promoting tissue regeneration were designed to minimize the host inflammatory response; although, recent appreciation for the roles that innate immune cells play in tissue repair and material integration has shifted this paradigm. A number of opportunities exist to exploit known signaling systems of specific populations of monocytes/macrophages to promote repair and to better understand the biological and pathological roles of myeloid cells. This review seeks to outline the characteristics of distinct populations of monocytes and macrophages, identify the role of these cells within diverse tissue injury niches, and offer design criteria for immunoregenerative biomaterials given the intrinsic inflammatory response to their implantation.

PLoS ONE ◽  
2019 ◽  
Vol 14 (3) ◽  
pp. e0213150 ◽  
Author(s):  
Federica De Santis ◽  
Noemi Poerio ◽  
Angelo Gismondi ◽  
Valentina Nanni ◽  
Gabriele Di Marco ◽  
...  

2019 ◽  
Vol 90 (e7) ◽  
pp. A42.3-A42
Author(s):  
Mastura Monif ◽  
Shokoufeh Abdollahi ◽  
Jim Stankovich ◽  
Vicki Maltby ◽  
Jeannette Lechner-Scott ◽  
...  

IntroductionCladribine Tablets (Mavenclad®) is nucleoside analogue of deoxyadenosine, and an oral treatment for relapsing remitting MS (RRMS). In RRMS clinical trials, Cladribine has been shown to reduce brain atrophy, relapse rates, and new lesions on brain MRI. P2X7R is a purinergic receptor expressed in innate immune cells, and is thought to play a critical role in neuroinflammation. The mechanism of action of Cladribine on peripheral innate immune cells (monocytes), and its effect on P2X7R, is unclear, and forms the basis of this study.MethodsThis will be a Phase IV, multi-centre, 3 year, translational trial. Patients who are starting Cladribine as part of their routine clinical care will consent to take part in the study. Monocyte numbers and activation states will be measured at various times prior and after commencement of therapy. In addition, and in an in vitro setting the effect of Cladribine on P2X7R expression and function will be assessed, as well as measuring various cytokines/chemokines in serum. The laboratory data will also be correlated with clinical data from another long-term Cladribine study, CLOBAS.ResultsThis study has been approved by Alfred Health Human Research Ethics Committee. The study is to commence in April 2019.ConclusionThis study will shed light on whether Cladribine is exerting its beneficial effects via action on peripheral monocytes and alterations of their P2X7Rs. The laboratory and clinical data will be analysed to understand the relationship between innate immune parameters and patient outcome.


Channels ◽  
2014 ◽  
Vol 8 (2) ◽  
pp. 131-141 ◽  
Author(s):  
Valentyna Maslieieva ◽  
Roger J Thompson

2013 ◽  
Vol 22 (12) ◽  
pp. 2367-2380 ◽  
Author(s):  
Hong Xu ◽  
Jun Yan ◽  
Ziqiang Zhu ◽  
Lala-Rukh Hussain ◽  
Yiming Huang ◽  
...  

2020 ◽  
Vol 131 ◽  
pp. 110497
Author(s):  
Bárbara Osmarin Turra ◽  
Fernanda Barbisan ◽  
Verônica Farina Azzolin ◽  
Cibele Ferreira Teixeira ◽  
Thamara Flores ◽  
...  

2020 ◽  
Vol 197 ◽  
pp. 108079 ◽  
Author(s):  
Rebecca Francis ◽  
Pawan Kumar Singh ◽  
Sukhvinder Singh ◽  
Shailendra Giri ◽  
Ashok Kumar

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Jing Wu ◽  
Xinping Lv ◽  
Shan Zhu ◽  
Tete Li ◽  
Hang Cheng ◽  
...  

Innate lymphoid cells (ILCs) comprise a recently identified subset of innate immune cells that are mainly localized to mucosa-associated tissues. Although they have not yet been fully characterized, they can generally be divided into ILC1s, ILC2s, and ILC3s. ILCs and their corresponding cytokines act as important mediators of the early stages of the immune response during inflammation, tissue repair, and the maintenance of epithelial integrity. Consequently, the dysregulation of ILC subsets might promote inflammation and cancer. Numerous studies have demonstrated that these cells play an important role in maintaining the microecological balance of the small intestine; however, their specific roles in mediating inflammation in this tissue and tumorigenesis remain unclear and controversial. In this review, we focus on recent progress that has helped to gain a better understanding of the role of ILCs in intestinal homeostasis, chronic inflammation, and cancer. Further focused research on the regulation and role of ILCs in intestinal homeostasis and pathology will help to reveal valuable diagnostic and therapeutic targets for the treatment of intestinal diseases.


Blood ◽  
2013 ◽  
Vol 122 (2) ◽  
pp. 243-252 ◽  
Author(s):  
Erika Zonari ◽  
Ferdinando Pucci ◽  
Massimo Saini ◽  
Roberta Mazzieri ◽  
Letterio S. Politi ◽  
...  

Key Points miR-155 knockdown in myeloid cells accelerates spontaneous breast cancer development. miR-155 is required by TAMs for deploying antitumoral activity.


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