Fcα receptor I (CD89) on neutrophils in periodontal lesions

Yuan, Zuan-Ning; Gjermo, Per; Helgeland, Kristen; Schenck, Karl

doi:10.1034/j.1600-051x.2000.027007489.x

Cited by 7 publications

(6 citation statements)

References 24 publications

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“…Our results revealed that CD68 + intestinal lamina propria macrophages failed to express CD89. These results are in agreement with previous observations that intestinal and gingival macrophages lack CD89 [34, 35]. Interestingly, macrophages isolated from the peritoneal cavity and bronchoalveolar lavage still expressed detectable levels of CD89 (and CD14), suggesting that these cells are less mature than those found in intestinal lamina propria or gingiva, perhaps owing to the lack of a tissue‐specific factor responsible for promoting terminal differentiation.…”

Section: Discussionsupporting

confidence: 92%

Expression and Modulation of the Human Immunoglobulin A Fc Receptor (CD89) and the FcR γ Chain on Myeloid Cells in Blood and Tissue

et al. 2003

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CD89, the human immunoglobulin A (IgA) Fc receptor (FcR), is a potential target for antibody-based therapeutics, but little is known about its expression and modulation in vivo. In this study, we examined the expression pattern of CD89 and its signalling subunit, the FcR g chain, on circulating myeloid cells and in various tissues. Our results showed a wide tissue distribution of CD89 þ cells. Thus, CD89 þ cells were evident as clusters in tonsils and appendix and scattered in varying numbers in lymph nodes, kidney, liver, intestinal mucosa, bronchoalveolar lavage and peritoneal fluid. Most CD89 þ cells were identified as neutrophils with high levels of CD89. A few recently emigrated macrophages (CD14 low ), weakly positive for CD89, were occasionally found in the tissues and more often in the peritoneal fluid. The level of CD89 on neutrophils in tissues and peripheral blood was similar, whereas on monocytes it was much lower in the tissues than in blood, and it was absent on CD14 -/CD68 þ intestinal lamina propria macrophages. Conversely, we detected much higher levels of the FcR g chain in monocytes than in neutrophils, but the FcR g chain was also downregulated in tissue macrophages as well as in in vitro-differentiated monocytederived macrophages and dendritic cells. The implications of our current findings on the biological functioning of CD89 are discussed.

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Section: Discussionsupporting

confidence: 92%

Expression and Modulation of the Human Immunoglobulin A Fc Receptor (CD89) and the FcR γ Chain on Myeloid Cells in Blood and Tissue

et al. 2003

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“…GCF PMN were found to exhibit higher levels of Fc␣RI and Fc␣RI-positive cells than PB PMN. These findings were in accordance with the results of immunohistochemical work showing that periodontal pocket areas were heavily infiltrated with Fc␣RI-expressing neutrophils (62). Fc␣RI expression on human PMN has been shown to be up-regulated by interleukin 8 (IL-8) (41), tumor necrosis factor alpha (TNF-␣) (26), and FMLP (25).…”

Section: Discussionsupporting

confidence: 85%

“…Consistently, mucosal phagocytes have been shown to exhibit an increased capacity to bind and ingest IgA-opsonized targets (14,25). Indeed, GCF PMN are immunocompetent cells that move from the bloodstream to mucosal sites (periodontal pocket), where subgingival plaque bacteria are coated with IgA (62). Fc␣R is expressed exclusively on phagocytes, whereas Fc␥R is more widely expressed on leukocytes (39).…”

Section: Discussionmentioning

confidence: 99%

Effective In Vitro Clearance ofPorphyromonas gingivalisby Fcα Receptor I (CD89) on Gingival Crevicular Neutrophils

et al. 2001

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Porphyromonas gingivalis has been implicated as a causative pathogen in periodontitis. Immunotherapeutic approaches have recently been suggested to aid in the clearance of P. gingivalis from disease sites. Because antibody-Fc receptor (FcR) interactions play a role in the effector functions of polymorphonuclear neutrophils (PMN), we evaluated which FcR on PMN from gingival crevicular fluid (GCF) serves as an optimal target molecule for FcR-directed immunotherapy. GCF PMN and peripheral blood (PB) PMN from adult periodontitis patients were analyzed for their immunoglobulin G (IgG) and IgA FcR (Fc␥R and Fc␣R, respectively) expression and function by studying IgG-and IgA-mediated elimination of P. gingivalis. GCF PMN exhibited higher Fc␣RI and Fc␥RI levels and lower Fc␥RIIa and Fc␥RIIIb levels than PB PMN. Functional studies revealed that GCF PMN exhibited less of a capacity to phagocytose and kill IgG1-opsonized P. gingivalis than PB PMN. IgA1-mediated phagocytosis and killing capacity was, however, comparable between GCF PMN and PB PMN. In summary, these in vitro results document that Fc␣RI represents a candidate target for FcRdirected immunotherapy for the clearance of P. gingivalis.

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“…Additionally, periodontal lesions were shown to contain significant levels of IgA and IgG antibody‐secreting cells (8). Moreover, dense infiltrates of PMNs with high expression levels of IgA and IgG Fc receptors (FcαR and FcγR) have been detected in the disease periodontium (9). FcαR or FcγR on PMNs may thus play a role in the pathogenesis of periodontitis.…”

Section: Distribution Of Immunoglobulin a Fc Receptor (Fcαri) Nt 324 mentioning

confidence: 99%

“…FcαRI expression levels on human PMNs have been shown to be upregulated by interleukin‐8 (27) and tumor necrosis factor‐α (28), both of which can be detected in inflamed gingival tissue of periodontitis patients (29, 30). Additionally, an immunohistochemical study documented periodontal pocket areas to be heavily infiltrated with FcαRI‐expressing neutrophils (9). Significant IgA levels specific to periodontal pathogens were observed in GCF and gingival tissue of periodontitis patients (6, 8).…”

Section: Distribution Of Immunoglobulin a Fc Receptor (Fcαri) Nt 324 mentioning

confidence: 99%

A novel polymorphism of FcαRI (CD89) associated with aggressive periodontitis

et al. 2004

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Immunoglobulin A Fc receptor (FcalphaRI) has been implicated in the pathogenesis of periodontitis, because increased IgA responses and FcalphaRI-bearing neutrophils are observed in the disease lesions. Inter-individual differences in susceptibility to periodontitis may be attributable to genetic variability in FcalphaRI-mediated immunity. We here identified an FcalphaRI novel polymorphism (nt 324 A-to-G transition) in the membrane-distal extracellular domain encompassing the ligand-binding site, not resulting in an amino acid change. We compared the FcalphaRI genotype distributions among 46 Japanese aggressive periodontitis (AGP) patients, 80 race-matched healthy controls (HCs), and 59 Caucasian HCs. No ethnic differences were observed in the FcalphaRI genotype distributions between Japanese and Caucasian HC. Notably, we observed a difference in the genotype distribution between the AGP and HC groups. Carriage rate of the nt 324 A allele was higher in the AGP (65.2%) than that in the HC group (42.5%) (odds ratio 2.54). Polymorphonuclear neutrophils from peripheral blood and gingival crevicular fluid exhibited a decreased phagocytosis of periodontopathic bacteria (Porphyromonas gingivalis) in the nt 324 A/A patients as compared with the nt 324 G/G patients. These results document a genetic polymorphism at the FcalphaRI ligand-binding site to be associated with susceptibility to AGP.

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Fcα receptor I (CD89) on neutrophils in periodontal lesions

Abstract: It is suggested that FcalphaRI on neutrophils may play an important rôle in elimination of IgA-opsonized bacteria, both in periodontal tissue and the adjacent pockets.

Cited by 7 publications

References 24 publications

Expression and Modulation of the Human Immunoglobulin A Fc Receptor (CD89) and the FcR γ Chain on Myeloid Cells in Blood and Tissue

Expression and Modulation of the Human Immunoglobulin A Fc Receptor (CD89) and the FcR γ Chain on Myeloid Cells in Blood and Tissue

Effective In Vitro Clearance ofPorphyromonas gingivalisby Fcα Receptor I (CD89) on Gingival Crevicular Neutrophils

A novel polymorphism of FcαRI (CD89) associated with aggressive periodontitis

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