Porphyromonas gingivalis interactions with complement receptor 3 (CR3): Innate immunity or immune evasion?

10.2741/2409 ◽  
2007 ◽  
Vol 12 (8-12) ◽  
pp. 4547 ◽  
Author(s):  
George Hajishengallis
Keyword(s):  
Innate Immunity ◽  
Porphyromonas Gingivalis ◽  
Immune Evasion ◽  
Complement Receptor ◽  
Complement Receptor 3

scholarly journals Subversion of Innate Immunity by Periodontopathic Bacteria via Exploitation of Complement Receptor-3

2008 ◽  
pp. 195-211 ◽  
Author(s):  
George Hajishengallis ◽  
Min Wang ◽  
Shuang Liang ◽  
Muhamad-Ali K. Shakhatreh ◽  
Deanna James ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Complement Receptor ◽  
Periodontopathic Bacteria ◽  
Complement Receptor 3

scholarly journals Vitamin D upregulates the macrophage complement receptor immunoglobulin in innate immunity to microbial pathogens

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Annabelle G. Small ◽  
Sarah Harvey ◽  
Jaspreet Kaur ◽  
Trishni Putty ◽  
Alex Quach ◽  
...  
Keyword(s):  
Vitamin D ◽  
Innate Immunity ◽  
Surface Expression ◽  
Microbial Pathogens ◽  
Cell Surface Expression ◽  
Complement Receptor ◽  
Hydroxyvitamin D ◽  
Dihydroxyvitamin D ◽  
Multistep Process ◽  
25 Hydroxyvitamin D

AbstractVitamin D deficiency remains a global concern. This ‘sunshine’ vitamin is converted through a multistep process to active 1,25-dihydroxyvitamin D3 (1,25D), the final step of which can occur in macrophages. Here we demonstrate a role for vitamin D in innate immunity. The expression of the complement receptor immunoglobulin (CRIg), which plays an important role in innate immunity, is upregulated by 1,25D in human macrophages. Monocytes cultured in 1,25D differentiated into macrophages displaying increased CRIg mRNA, protein and cell surface expression but not in classical complement receptors, CR3 and CR4. This was associated with increases in phagocytosis of complement opsonised Staphylococcus aureus and Candida albicans. Treating macrophages with 1,25D for 24 h also increases CRIg expression. While treating macrophages with 25-hydroxyvitamin D3 does not increase CRIg expression, added together with the toll like receptor 2 agonist, triacylated lipopeptide, Pam3CSK4, which promotes the conversion of 25-hydroxyvitamin D3 to 1,25D, leads to an increase in CRIg expression and increases in CYP27B1 mRNA. These findings suggest that macrophages harbour a vitamin D-primed innate defence mechanism, involving CRIg.

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)

scholarly journals Mechanisms by which Porphyromonas gingivalis evades innate immunity

PLoS ONE ◽  
2017 ◽  
Vol 12 (8) ◽  
pp. e0182164 ◽  
Author(s):  
Kaveh Abdi ◽  
Tsute Chen ◽  
Brian A. Klein ◽  
Albert K. Tai ◽  
Jill Coursen ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Porphyromonas Gingivalis

scholarly journals Transmembrane segments of complement receptor 3 do not participate in cytotoxic activities but determine receptor structure required for action ofBordetellaadenylate cyclase toxin

2016 ◽  
Vol 74 (3) ◽  
pp. ftw008 ◽  
Author(s):  
Tomas Wald ◽  
Adriana Osickova ◽  
Jiri Masin ◽  
Petra M. Liskova ◽  
Inga Petry-Podgorska ◽  
...  
Keyword(s):  
Cytotoxic Activities ◽  
Complement Receptor ◽  
Transmembrane Segments ◽  
Receptor Structure ◽  
Complement Receptor 3

CD209 (DC-SIGN) – role in the work of the innate immunity and pathogen penetration

2020 ◽  
Vol 1 (9) ◽  
pp. 64-71
Author(s):  
E. A. Klimov ◽  
◽  
E. K. Novitskaya ◽  
S. N. Koval’chuk ◽  
◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immunity ◽  
Dendritic Cells ◽  
Inflammatory Response ◽  
Signaling Pathway ◽  
Adhesion Molecule ◽  
Immune Evasion ◽  
Intercellular Adhesion Molecule ◽  
Lectin Receptor

Intercellular adhesion molecule CD209 (DC-SIGN) is a membrane C-type lectin receptor expressed on the surface of dendritic cells and macrophages. CD209 plays an important role in innate immunity. Many studies have shown the possibility of interaction of the CD209 molecule with a number of dangerous pathogens of humans and animals. This review summarizes information on the structure of the CD209 gene and its product, describes the role of the CD209 protein in the immune response, in the migration of dendritic cells from the blood to the tissue, and their interaction with neutrophils. The currently known signaling pathway of activation through the CD209 inflammatory response is presented. The role of CD209 as an endocytic antigen receptor and the participation of the protein in immune evasion of pathogens are discussed. The mechanisms known to date for the development of infections caused by pathogens of various nature in animals are described.

scholarly journals Activated microglia desialylate their surface, stimulating complement receptor 3‐mediated phagocytosis of neurons

Glia ◽  
2019 ◽  
Vol 68 (5) ◽  
pp. 989-998 ◽  
Author(s):  
David H. Allendorf ◽  
Mar Puigdellívol ◽  
Guy C. Brown
Keyword(s):  
Complement Receptor ◽  
Activated Microglia ◽  
Complement Receptor 3
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