Fcγ-receptor IIA genotype and invasive pneumococcal infection

Moens, Leen; Hoeyveld, Ernestina Van; Verhaegen, Jan; Boeck, K. De; Peetermans, Willy; Bossuyt, Xavier

doi:10.1016/j.clim.2005.08.002

Cited by 36 publications

(35 citation statements)

References 28 publications

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“…The lack of association of Fc␥RIIa-R/R131 genotype with increased susceptibility to respiratory infections is consistent with previous observations in invasive pneumococcal disease (20 ).…”

Section: Discussionsupporting

confidence: 92%

“…The distribution of the Fc␥RIIa genotypes in the control popClinical Chemistry 53, No. 1,2007 ulation (n ϭ 43) was comparable to the distribution in a larger control population (20 ).…”

Section: Genotyping Of Mbl2 Fc␥riia and C2supporting

confidence: 51%

“…Genotyping of Fc␥RIIa was as described (20 ). The distribution of the Fc␥RIIa genotypes in the control popClinical Chemistry 53, No.…”

Section: Genotyping Of Mbl2 Fc␥riia and C2mentioning

confidence: 99%

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Coexistence of (Partial) Immune Defects and Risk of Recurrent Respiratory Infections

Bossuyt¹,

Moens²,

Hoeyveld³

et al. 2007

Clinical Chemistry

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Background: Respiratory infections are major causes of morbidity and mortality, but determinants of susceptibility are poorly defined. We studied whether and to what extent immunologic and genetic factors are associated with increased susceptibility to respiratory infections. Methods: We evaluated the prevalence of IgA, IgM, IgG, and IgG subclass deficiencies, impairment in the antibody response against pneumococcal polysaccharides, G2m(n) allotypes, Fc␥RIIa polymorphisms, partial C2 and partial C4 deficiency, promoter polymorphisms in MBL2, and lymphocyte subset deficiencies in a control population and in consecutive children with recurrent respiratory infections. Results: IgA and/or IgG subclass deficiency was found in 27 of 55 patients (49%) and 6 of 43 controls (14%) (P ‫؍‬ 0.0006). An impaired antibody response to polysaccharides was found in 7 patients (19%) and in 0 of 37 controls (P ‫؍‬ 0.002). The Gm(n)marker was absent in 25 of 55 patients (45%) and 6 of 42 controls (14%) (P ‫؍‬ 0.009). The MBL2 variants O/O, A/O, and A/A occurred in 9, 14, and 32 of the 55 patients, respectively, and in 1, 19, and 23 of the 43 controls, respectively (P ‫؍‬ 0.05). There was no increase in the prevalence of partial C4 deficiency, C2 deficiency, lymphocyte subset deficiency, or Fc␥RIIa polymorphism in the patients compared to the controls. A combination of at least 2 immune defects was found in 31 of 55 patients (56%) and in 4 of 42 controls (11.6%) (P <0.0001). Conclusion: Specific antipolysaccharide antibody deficiency, IgA and/or IgG subclass deficiency, Gm(n) allotype, and MBL2 genotype are susceptibility factors for recurrent respiratory infections, and coexistence of sev-

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Section: Discussionsupporting

confidence: 92%

“…The distribution of the Fc␥RIIa genotypes in the control popClinical Chemistry 53, No. 1,2007 ulation (n ϭ 43) was comparable to the distribution in a larger control population (20 ).…”

Section: Genotyping Of Mbl2 Fc␥riia and C2supporting

confidence: 51%

See 1 more Smart Citation

Coexistence of (Partial) Immune Defects and Risk of Recurrent Respiratory Infections

Bossuyt¹,

Moens²,

Hoeyveld³

et al. 2007

Clinical Chemistry

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“…For example, individuals with the RR genotype have about a 1.5-fold increased risk of systemic lupus erythematosus than do individuals with the HH genotype (30). Some studies, but not others, have found an increased risk of invasive pneumococcal or meningococcal disease with the RR genotype (31,32,41,42). In contrast, RR patients may be protected from severe malaria (33).…”

Section: Discussionmentioning

confidence: 99%

FcγRIIa Genotype Predicts Progression of HIV Infection

Forthal

Landucci

Bream

et al. 2007

The Journal of Immunology

119

129

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Polymorphisms in FcγR genes are associated with susceptibility to or severity of a number of autoimmune and infectious diseases. We found that HIV-infected men in the Multicenter AIDS Cohort Study with the FcγRIIa RR genotype progressed to a CD4+ cell count of <200/mm3 at a faster rate than individuals with the RH or HH genotypes (relative hazard = 1.6; p = 0.0001). However, progression to AIDS (using the broad definition of either a CD4+ cell count <200/mm3 or development of an AIDS-defining illness) was less impacted by FcγRIIa genotype, largely because HH homozygotes had an increased risk of Pneumocystis jiroveci pneumonia as an AIDS-defining illness. We also showed that chronically infected subjects develop a substantial anti-gp120-specific IgG2 response. Moreover, HIV-1 immune complexes are more efficiently internalized by monocytes from HH subjects compared with RR subjects, likely because of the presence of IgG2 in the complexes. Finally, the FcγRIIIa F/V gene polymorphism was not associated with progression of HIV infection, but, as demonstrated previously, did predict the risk of Kaposi’s sarcoma. These results demonstrate the importance of FcγRs in AIDS pathogenesis and point toward a critical role for interactions between FcγRs and immune complexes in disease progression.

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“…Both S. pneumoniae and H. influenzae are surrounded by a polysaccharide capsule that protects the bacteria from phagocytosis. However, if immunoglobulin G2 (IgG2) subclass antibodies recognize and bind capsular polysaccharide antigens, opsonophagocytosis can take place (7,11,12). The only receptor able to interact efficiently with IgG2 antibodies is Fc␥ receptor IIa (Fc␥-RIIa; CD32).…”

mentioning

confidence: 99%

The Fcγ Receptor IIA-R/R131 Genotype Is Associated with Severe Sepsis in Community-Acquired Pneumonia

Endeman

Cornips

Grutters

et al. 2009

Clin Vaccine Immunol

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Community-acquired pneumonia (CAP) can be caused by a variety of microorganisms but is most frequently associated with Streptococcus pneumoniae and gram-negative bacteria like Haemophilus influenzae. Encapsulated bacteria are able to escape phagocytosis, unless they are bound by immunoglobulin G2 subclass antibodies. These antibodies interact with Fc␥ receptor IIa (Fc␥-RIIa), thereby facilitating opsonophagocytosis of the encapsulated bacteria. We studied the relationship between the Fc␥-RIIa-R/H131 polymorphism and the clinical course of CAP and pathogen-specific susceptibility. Regarding methodology, the Fc␥-RIIa genotype R/H131 was determined in 200 patients with CAP and in 313 healthy controls and was correlated with the clinical course, laboratory parameters, and causative microorganism. The Fc␥-RIIa-R/R131 genotype was found more frequently in patients with severe sepsis (odds ratio [OR], 2.55; 95% confidence interval [CI], 1.30 to 5.00; P < 0.01). The majority of patients in this group suffered from invasive pneumococcal disease. The duration of hospital stay was longer for patients with the Fc␥-RIIa-R/R131 genotype. Fc␥-RIIa genotypes were not associated with an increased risk of CAP in general; however, the Fc␥-RIIa-R/R131 genotype was found more frequently in patients with CAP caused by H. influenzae than in controls (OR, 3.03; CI, 1.04 to 9.09; P < 0.05). In conclusion, the Fc␥-RIIa-R/R131 genotype is associated with severity of CAP and is more frequent in CAP caused by H. influenzae.

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Fcγ-receptor IIA genotype and invasive pneumococcal infection

Cited by 36 publications

References 28 publications

Coexistence of (Partial) Immune Defects and Risk of Recurrent Respiratory Infections

Coexistence of (Partial) Immune Defects and Risk of Recurrent Respiratory Infections

FcγRIIa Genotype Predicts Progression of HIV Infection

The Fcγ Receptor IIA-R/R131 Genotype Is Associated with Severe Sepsis in Community-Acquired Pneumonia

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