Meningococcal disease and polymorphism of FcγRIIa (CD32) in late complement component-deficient individuals

Platonov, Alexander E.; Kuijper, Ed J.; Vershinina, I. V.; Shipulin, German A.; Westerdaal, N. A. C.; Fijen, C. A. P.; Winkel, Jan G. J. van de

doi:10.1046/j.1365-2249.1998.00484.x

Cited by 54 publications

(32 citation statements)

References 22 publications

(27 reference statements)

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“…FcγRIIa genotyping was performed as described earlier [7, 8]. The cells of only one donor, A.E.P., were used throughout the study to minimize interassay variations.…”

Section: Methodsmentioning

confidence: 99%

“…The importance of phagocytosis is less clear. We have demonstrated that both complement-sufficient and complement-deficient individuals, having FcγRIIa-H/H131 allotype of leukocyte FcγRIIa IgG receptor, also had a decreased probability to contract severe meningococcal disease [7, 8]. Because human polymorphonuclear leukocytes (PMNL) bearing FcγRIIa-H/H131 allotype are more effective in IgG2-dependent opsonophagocytosis in vitro and because most anticapsular meningococcal antibodies in vivo belong to IgG2 isotype, these findings suggest that the efficiency of phagocytosis may influence the prevalence and severity of meningococcal disease.…”

Section: Introductionmentioning

confidence: 99%

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Antibody-Dependent Killing of Meningococci by Human Neutrophils in Serum of Late Complement Component-Deficient Patients

Platonov

Vershinina²,

Käyhty³

et al. 2003

Int Arch Allergy Immunol

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Background: Thirty-one Russian patients with late complement component deficiency (LCCD) who had experienced one to five meningococcal infections were immunized with meningococcal polysaccharide vaccine (A + C + W135 + Y) and were followed for 3–8 years. We investigated the potentially protective killing effect of human neutrophils (PMNL) on serogroup A and W135 meningococci. Methods: Meningococci were incubated in LCCD vaccinee sera in the absence or presence of PMNL, and the number of live bacteria (CFU) was determined by plating onto chocolate agar. Results: When meningococci were incubated in the LCCD sera alone, exponential growth of meningococci occurred despite the presence of meningococcal antibodies. After the addition of PMNL, meningococci were inhibited in their growth or even eliminated. Group A or W135 meningococci were killed effectively by PMNL in 80% of the sera which were collected 1 month to 1 year after vaccination compared to only 40% in the prevaccination LCCD sera (p < 0.05). Three years after vaccination 67% of the LCCD sera were still capable of promoting killing (and even 90% after revaccination). The rate of killing correlated with the concentration of serogroup-specific immunoglobulins. In 83% of the 72 LCCD sera with more than 5 µg/ml anti-group A immunoglobulins the killing of group A meningococci was promoted. By contrast, only 21% of 19 samples with lower specific antibody levels showed a PMNL-mediated meningococcal killing (p < 0.05). The same effect was observed for group W135 meningococci. Conclusion: PMNL kill meningococci during incubation in LCCD serum; this effect increases after vaccination and depends on both specific antibody and complement. Protection by vaccination may therefore be caused by an increased killing capacity of PMNL.

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“…FcγRIIa genotyping was performed as described earlier [7, 8]. The cells of only one donor, A.E.P., were used throughout the study to minimize interassay variations.…”

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Antibody-Dependent Killing of Meningococci by Human Neutrophils in Serum of Late Complement Component-Deficient Patients

Platonov

Vershinina²,

Käyhty³

et al. 2003

Int Arch Allergy Immunol

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“…[7][8][9] Its role is even more significant in complement deficiency where phagocytosis depends mainly on Fc␥Rs. 10 Understanding the regulation of Fc␥RIIA gene expression in myeloid cells may provide a means for controlling innate immunity.…”

Section: Introductionmentioning

confidence: 99%

Induction of FcγRIIA expression in myeloid PLB cells during differentiation depends on cytosolic phospholipase A2 activity and is regulated via activation of CREB by PGE2

Hazan-Eitan

Weinstein

Hadad

et al. 2006

Blood

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FcγRIIA expressed on neutrophils and monocytes has a fundamental role in combating bacterial infections. In the present study, the requirement of cytosolic phospholipase A2 (cPLA2) for induction of FcγRIIA expression was studied in a model of cPLA2-deficient PLB-985 cells (PLB-D cells). FcγRIIA was acquired only during differentiation of PLB but not of PLB-D cells induced by either 1,25-dihydroxyvitamin D3, retinoic acid, or interferon γ. Addition of prostaglandin E2 (PGE2) to PLB-D cells undergoing differentiation restored the expression of FcγRIIA protein, whereas addition of indomethacin to PLB cells during differentiation inhibited both the production of PGE2 and the expression of FcγRIIA. Inhibition of PKA during PLB differentiation prevented FcγRIIA expression, whereas dibutyryl cAMP (dbcAMP) induced its expression in both PLB and PLB-D cells. CREB phosphorylation and CREB-CRE interaction were detected only in differentiated PLB cells and not PLB-D cells and were inhibited by indomethacin. A reporter gene containing a FcγRIIA gene promoter fragment with the CRE element was sufficient for CREB activation. Our results are the first to show that CREB activation is involved in up-regulation of FcγRIIA expression in myeloid lineages. PGE2 formed via cPLA2 activates CREB through PKA and this process is dependent on development of PGE2 receptor 4.

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“…Most studies have demonstrated higher frequencies of the Fc RIIa-R131/R131 or Fc RIIIb-NA2/NA2 genotypes in patients with meningococcal disease [178][179][180][181][182][183][184] particularly in patients with severe meningococcal disease or fulminant meningococcal septic shock. The Fc RIIa polymorphism has also been demonstrated to be associated with infections due to other encapsulated bacteria [185,186].…”

Section: Fcmentioning

confidence: 99%

Host Genetics and Pediatric Sepsis

Quasney¹

2011

TOINFJ

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Susceptibility to, and outcome from, sepsis in children is highly variable due in part to genetic variation in genes coding for components of the innate immune response. This review article will discuss evidence for the influence of host genetic variability on the susceptibility to, and outcome from, sepsis in children and adults. Polymorphisms in genes coding for proteins involved in the recognition of bacterial pathogens (TLR4, CD-14, Fc RIIa, and mannose binding lectin) and the response to bacterial pathogens (TNF-, IL-1 , IL-1 , IL-1 RA , IL-6, IL-10, heat shock proteins, ACE, plasminogen activator inhibitor-1) can influence the amount or function of the protein produced in response to bacterial stimuli. Evidence is discussed suggesting that some of these genetic polymorphisms influence the susceptibility to, and outcome from, sepsis. Conclusion:Host genetic variability in the regulatory and coding regions of genes for components of the innate immune system may influence the susceptibility to and/or outcome from sepsis. The disparate results observed in many studies of polymorphisms in sepsis emphasize the need for future studies to be larger, to include the analysis of multiple polymorphisms, and to be better designed with respect to control populations in order to identify the degree of influence that genetic variability has on sepsis.

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Meningococcal disease and polymorphism of FcγRIIa (CD32) in late complement component-deficient individuals

Cited by 54 publications

References 22 publications

Antibody-Dependent Killing of Meningococci by Human Neutrophils in Serum of Late Complement Component-Deficient Patients

Antibody-Dependent Killing of Meningococci by Human Neutrophils in Serum of Late Complement Component-Deficient Patients

Induction of FcγRIIA expression in myeloid PLB cells during differentiation depends on cytosolic phospholipase A2 activity and is regulated via activation of CREB by PGE2

Host Genetics and Pediatric Sepsis

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