Microglia and Macrophage Activation and the Regulation of Complement-Receptor-3 (CR3/MAC-1)-Mediated Myelin Phagocytosis in Injury and Disease

2003 ◽  
Vol 21 (1) ◽  
pp. 65-72 ◽  
Author(s):  
Shlomo Rotshenker
Keyword(s):  
Macrophage Activation ◽  
Complement Receptor ◽  
Myelin Phagocytosis ◽  
Complement Receptor 3

Modulation (Inhibition and Augmentation) of Complement Receptor-3-Mediated Myelin Phagocytosis

2001 ◽  
Vol 8 (3) ◽  
pp. 504-512 ◽  
Author(s):  
Fanny Reichert ◽  
Uri Slobodov ◽  
Chen Makranz ◽  
Shlomo Rotshenker
Keyword(s):  
Complement Receptor ◽  
Myelin Phagocytosis ◽  
Complement Receptor 3

Galectin-3/MAC-2, Ras and PI3K activate complement receptor-3 and scavenger receptor-AI/II mediated myelin phagocytosis in microglia

Glia ◽  
2008 ◽  
Vol 56 (15) ◽  
pp. 1607-1613 ◽  
Author(s):  
Shlomo Rotshenker ◽  
Fanny Reichert ◽  
Miri Gitik ◽  
Ronit Haklai ◽  
Galit Elad-Sfadia ◽  
...  
Keyword(s):  
Scavenger Receptor ◽  
Complement Receptor ◽  
Myelin Phagocytosis ◽  
Galectin 3 ◽  
Complement Receptor 3

scholarly journals β-Glucan enhances complement-mediated hematopoietic recovery after bone marrow injury

Blood ◽  
2006 ◽  
Vol 107 (2) ◽  
pp. 835-840 ◽  
Author(s):  
Daniel E. Cramer ◽  
Daniel J. Allendorf ◽  
Jarek T. Baran ◽  
Richard Hansen ◽  
Jose Marroquin ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mouse Serum ◽  
Complement Receptor ◽  
Dependent Manner ◽  
Complement Receptor 3 ◽  
Total Body ◽  
Stimulating Factor ◽  
Sublethal Irradiation ◽  
Classic Pathway

AbstractMyelotoxic injury in the bone marrow (BM) as a consequence of total body irradiation (TBI) or granulocyte colony-stimulating factor (G-CSF) mobilization results in the deposition of iC3b on BM stroma (stroma-iC3b). In the present study, we have examined how stroma-iC3b interacts with hematopoietic progenitor cells (HPCs) and the role of complement (C) and complement receptor 3 (CR3) in BM injury/repair. We demonstrate here that stroma-iC3b tethers HPCs via the inserted (I) domain of HPC complement receptor 3 (CR3, CD11b/CD18, Mac-1). Following irradiation, stroma-iC3b was observed in the presence of purified IgM and normal mouse serum (NMS), but not serum from Rag-2-/- mice, implicating a role for antibody (Ab) and the classic pathway of C activation. Furthermore, a novel role for soluble yeast β-glucan, a ligand for the CR3 lectin-like domain (LLD), in the priming of CR3+ HPC is suggested. Soluble yeast β-glucan could enhance the proliferation of tethered HPCs, promote leukocyte recovery following sublethal irradiation, and increase the survival of lethally irradiated animals following allogeneic HPC transplantation in a CR3-dependent manner. Taken together, these observations suggest a novel role for C, CR3, and β-glucan in the restoration of hematopoiesis following injury. (Blood. 2006;107:835-840)

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