Browse our CD16 Molecule Proteins (CD16)

Cow (Bovine) CD16 Molecule (CD16) interaction partners

1. cytotoxic role of lymph node residing NK cells, beyond the predominantly cytokine-producing role previously inferred from studies on human NK cells

Human CD16 Molecule (CD16) interaction partners

1. Collectively, these results indicate that the amino acid substitution Ala78Asp resulting in the HNA-1c allotype leads to higher affinity toward human IgG, enhancement of neutrophil activation, and possibly effective clearance of malaria by intracellular reactive oxygen species.

2. SHP-2 is activated by CD16b crosslinking in neutrophils.

3. FCGR3B deficiency due to copy number variations may predispose to eosinophilic granulomatosis with polyangiitis.

4. low copy numbers of FCGR2A and FCGR3B to be common risk factors for systemic lupus nephritis (SLE) and ANCA-associated systemic vasculitis (AASV).

5. The FCGR3B NA1/NA1 genotype is associated with hypersensitivity reactions to adalimumab in Japanese patients with Rheumatoid Arthritis.

6. Data suggest association of FCGR3B deletion with increased risk of rheumatoid arthritis (RA) in a large cohort.

7. Gene copy number variation (CNV) of the PKLR, FCGR2A, FCGR2C, and FCGR3 genes is associated with malaria severity, and our results provide evidence for a role of CNV in host responses to malaria.

8. Association between Fc gamma Receptor IIIB genetic polymorphisms and susceptibility to severe malaria anemia in children in western Kenya.

9. We conclude that FCGR3A CNVs are a major risk factor for female sarcoidosis and FCGR3B CNVs may also affect the development of sarcoidosis.

10. CD16 and CD35 are important for neutrophil internalization of M. tuberculosis, whereas HIV-1 infection adversely affects opsonophagocytosis.

11. There was no aberration in FCGR3B allele/genotype frequencies in sarcoidosis patients compared to controls.

12. Results showed that susceptibility to systemic lupus erythematosus was associated with the FCGR3B*01 allele, as well as with the FCGR3B*01/*01 and FCGR3B*01/*02 genotypes.

13. FcgammaRIIIB allelic distribution was similar among pediatric Guillain-Barre syndrome patients and controls.

14. Lower copy numbers (

15. This metaanalysis indicates that polymorphisms in the pathways of immune complex clearance, such as the FcgammaRIIIa, FcgammaRIIIb, and ITGAM genotypes, are potential susceptibility genes for neuropsychiatric systemic lupus erythematosus.

16. data show that cross-linking FcgammaRIIIb is responsible for NET formation by the human neutrophil

17. our method allows determining the CNV status of the FCGR locus, we identified association of CNV in FCGR3B to RA and showed a functional relationship between CNV in the FCGR3A gene and CD16A expression.

18. Fc-gamma receptor polymorphisms differentially influence susceptibility to systemic lupus erythematosus and lupus nephritis.

19. the results of this meta-analysis indicated that low FCGR3B CN increased susceptibility to autoimmune diseases--{REVIEW}

20. Data show that gains or losses in copy numbers of Fc gamma receptors FCGR3A were less frequent than for FCGR3B and FCGR2C.

Mouse (Murine) CD16 Molecule (CD16) interaction partners

1. Although enhanced humoral immune responses were observed in the absence of FcgammaRIIIA in the mouse asthma model, no overall regulation by FcgammaRIIIA, especially in terms of those parameters measuring lung tissue inflammation, was recorded. In the absence of FcgammaRIIB, augmented immune responses measured as serum antibody levels as well as those in various regulatory pathways in this mouse asthma model were observed.

2. FcgammaRIIb and FcgammaRIII are involved in the CRP-induced expression of MMPs and TIMP-1 and the CRP-induced phosphorylation of p38, whereas the FcgammaR-independent pathway may regulate the CRP-induced MMP-11 expression and the CRP-induced ERK1/2 phosphorylation.

3. PLCd1 negatively regulates lipopolysaccharide-induced production of IL-1b and Fc gamma receptor-mediated phagocytosis in macrophages.

4. Meanwhile, the observed reduction in the phagocytic activity of the MafB-shRNA-expressing cells was attenuated by ectopic expression of Fcgr3. Together, the results presented here indicate that MafB influences the phagocytic activity of macrophages by promoting Fcgr3, but not Fcgr2b, expression.

5. Fcgr3 resided in Kupffer cells, and it contributed to the inhibition of the growth of liver tumor cells.

6. FcgammaRIII knockout mice displayed significantly less cellular infiltration in the lungs after hRSV infection, compared with wild-type mice, suggesting a potentially harmful, IgG-independent role for this receptor in hRSV disease.

7. Nlrp3-inflammasome and FcgammaRIII have roles in Dengue virus and antiplatelet autoantibody-induced hemorrhage

8. FcgammaRIII inhibits osteoclastogenesis by depriving other osteoclastogenic Ig-like receptors of FcRgamma.

9. Data show that mast cells (MC) FcgammaRIII-induced degranulation promotes antibody-enhanced vascular leakage.

10. Fcgamma-RII and Fcgamma-RIII might participate in the uptake and/or transport of IgG through the intestinal epithelia of adult mice.

11. Scavenger receptor function of mouse Fcgamma receptor III contributes to progression of atherosclerosis in apolipoprotein E hyperlipidemic mice.

12. These results suggest that respiratory syncytial virus persistence in macrophages induce intracellular effects that have an impact on Fcgamma receptor gene expression at both mRNA and protein levels.

13. Antitumor activities of agonistic anti-TNFR antibodies require differential FcgammaRIIB coengagement in vivo.

14. These data demonstrate the initiation of endothelial barrier dysfunction in vitro and in vivo by direct binding of anti-HNA-3a on endothelial cells.

15. Absence of FcgammaRIII in heart transplantation is associated with enhanced inflammation, alloantibody production, and complement activation leading to accelerated cardiac allograft rejection.

16. allergen-specific IgG can enhance secondary responses by ligating FcgammaRIII on antigen-presenting cells to augment development of Th2-mediated responses in the lungs via an IL-33-dependent mechanism

17. FcgammaRIII contributes to a therapy model of B16 lung metastases; activating IgG receptors are necessary for the protective effect of monoclonal antibody.

18. NKG2D-mediated, but not Fc receptor-mediated, recognition increases natural killer (NK) cell degranulation; only NKG2D engagement substantially enhances degranulation.

19. The mechanism(s) of phagocytosis in the second phase of blood incompatibility reaction required neither C3 nor FcgammaRs

20. Our findings reveal a fine-tuning system for regulating mast cell apoptosis through aggregating FcgammaRIIB and Fcgamma RIIIA receptors by IgG immune complexes.