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Background: Naturally-acquired immunity to Plasmodium falciparum malaria develops after several episodes of infection. Fc gamma receptors (FcγRs) bind to immunoglobulin G (IgG) antibodies and mediate phagocytosis of opsonized microbes, thereby, linking humoral and cellular immunity. FcγR polymorphisms influence binding affinity to IgGs and consequently, can influence clinical malaria outcomes. Specifically, variations in FcγRIIA -131Arg/His, FcγRIIIA-176F/V and FcγRIIIB-NA1/NA2 modulate immune responses through altered binding preferences to IgGs and immune complexes. Differential binding, in turn, changes ability of immune cells to respond to infection through production of inflammatory mediators during P. falciparum infection.

Methods: We determined the association between haplotypes of FcγRIIA-131Arg/His, FcγRIIIA-176F/V and FcγRIIIB-NA1/NA2 variants and severe malarial anemia (SMA; hemoglobin < 6.0 g/dL, any density parasitemia) in children (n = 274; aged 6-36 months) presenting for their first hospital visit with P. falciparum malaria in a holoendemic transmission region of western Kenya. FcγRIIA-131Arg/His and FcγRIIIA-176F/V genotypes were determined using TaqMan® SNP genotyping, while FcγRIIIBNA1/NA2 genotypes were determined using restriction fragment length polymorphism. Hematological and parasitological indices were measured in all study participants.

Results: Carriage of FcγRIIA-131Arg/FcγRIIIA-176F/FcγRIIIBNA2 haplotype was associated with susceptibility to SMA (OR = 1.70; 95% CI; 1.02-2.93; P = 0.036), while the FcγRIIA-131His/ FcγRIIIA-176F/ FcγRIIIB NA1 haplotype was marginally associated with enhanced susceptibility to SMA (OR: 1.80, 95% CI; 0.98-3.30, P = 0.057) and higher levels of parasitemia (P = 0.009). Individual genotypes of FcγRIIA-131Arg/His, FcγRIIIA-176F/V and FcγRIIIB-NA1/NA2 were not associated with susceptibility to SMA.

Conclusion: The study revealed that haplotypes of FcγRs are important in conditioning susceptibility to SMA in immune-naive children from P. falciparum holoendemic region of western Kenya.

Titel:	Association between Fcγ receptor IIA, IIIA and IIIB genetic polymorphisms and susceptibility to severe malaria anemia in children in western Kenya.
Autor/in / Beteiligte Person:	Munde, EO ; Okeyo, WA ; Raballah, E ; Anyona, SB ; Were, T ; Ong'echa, JM ; Perkins, DJ ; Ouma, C
Link:	Zum Volltext
Zeitschrift:	BMC infectious diseases, Jg. 17 (2017-04-20), Heft 1, S. 289
Veröffentlichung:	London : BioMed Central, [2001-, 2017
Medientyp:	academicJournal
ISSN:	1471-2334 (electronic)
DOI:	10.1186/s12879-017-2390-0
Schlagwort:	Anemia etiology Child, Preschool Cross-Sectional Studies Female GPI-Linked Proteins genetics Genetic Predisposition to Disease Genotype Haplotypes Humans Infant Kenya Malaria genetics Malaria, Falciparum blood Malaria, Falciparum complications Male Parasite Load Polymorphism, Restriction Fragment Length Anemia genetics Malaria complications Polymorphism, Genetic Receptors, IgG genetics
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article Language: English [BMC Infect Dis] 2017 Apr 20; Vol. 17 (1), pp. 289. <i>Date of Electronic Publication: </i>2017 Apr 20. MeSH Terms: Polymorphism, Genetic* ; Anemia / genetics ; Malaria / complications ; Receptors, IgG / *genetics ; Anemia / etiology ; Child, Preschool ; Cross-Sectional Studies ; Female ; GPI-Linked Proteins / genetics ; Genetic Predisposition to Disease ; Genotype ; Haplotypes ; Humans ; Infant ; Kenya ; Malaria / genetics ; Malaria, Falciparum / blood ; Malaria, Falciparum / complications ; Male ; Parasite Load ; Polymorphism, Restriction Fragment Length References: J Clin Microbiol. 2011 Feb;49(2):671-6. (PMID: 21106789) ; Hum Genet. 2012 Feb;131(2):289-99. (PMID: 21818580) ; Lancet. 2002 Apr 13;359(9314):1311-2. (PMID: 11965279) ; AIDS. 2006 Jan 9;20(2):275-80. (PMID: 16511422) ; Am J Trop Med Hyg. 2006 Mar;74(3):376-85. (PMID: 16525094) ; Transfusion. 1995 Jan;35(1):54-7. (PMID: 7998071) ; Acta Trop. 2008 Feb;105(2):191-5. (PMID: 18022136) ; Am J Trop Med Hyg. 2006 Apr;74(4):573-7. (PMID: 16606986) ; Scand J Immunol. 2007 Jul;66(1):87-96. (PMID: 17587350) ; J Clin Invest. 1997 Sep 1;100(5):1059-70. (PMID: 9276722) ; J Clin Invest. 1990 Apr;85(4):1287-95. (PMID: 1690757) ; J Leukoc Biol. 2014 Dec;96(6):1131-42. (PMID: 25118179) ; Nature. 2002 Feb 7;415(6872):673-9. (PMID: 11832955) ; Malar J. 2005 Dec 01;4:56. (PMID: 16321150) ; Parasitol Int. 2002 Dec;51(4):361-6. (PMID: 12421634) ; N Engl J Med. 1995 May 25;332(21):1399-404. (PMID: 7723795) ; Hum Hered. 2006;61(1):10-4. (PMID: 16514241) ; Trends Parasitol. 2001 Nov;17(11):545-51. (PMID: 11872400) ; Immunology. 1994 Dec;83(4):624-30. (PMID: 7875742) ; Proc Natl Acad Sci U S A. 2012 Oct 16;109(42):16786-93. (PMID: 22949651) ; J Exp Med. 1989 Aug 1;170(2):481-97. (PMID: 2526846) ; Blood. 1997 Aug 1;90(3):1109-14. (PMID: 9242542) ; Lab Invest. 2000 May;80(5):617-53. (PMID: 10830774) ; Am J Trop Med Hyg. 2003 Dec;69(6):565-8. (PMID: 14740869) ; Infect Genet Evol. 2014 Apr;23:169-75. (PMID: 24594077) ; PLoS One. 2010 Mar 25;5(3):e9871. (PMID: 20360847) ; Blood. 1999 Jan 1;93(1):357-62. (PMID: 9864181) ; Blood. 1994 Sep 15;84(6):1753-9. (PMID: 7521687) ; Arthritis Rheum. 2006 Dec;54(12):3908-17. (PMID: 17133600) ; Blood. 2000 Apr 1;95(7):2386-90. (PMID: 10733511) ; Trends Immunol. 2003 Jan;24(1):30-5. (PMID: 12495722) ; Annu Rev Cell Dev Biol. 1996;12:181-220. (PMID: 8970726) ; J Immunol. 1991 Aug 15;147(4):1338-43. (PMID: 1831223) ; BMC Biotechnol. 2011 Jul 22;11:77. (PMID: 21781305) ; Infect Immun. 2000 Mar;68(3):1252-8. (PMID: 10678934) ; Br J Haematol. 2006 Apr;133(2):206-9. (PMID: 16611313) ; Annu Rev Immunol. 1991;9:457-92. (PMID: 1910686) ; Immunol Today. 1993 May;14(5):215-21. (PMID: 8517920) ; J Clin Invest. 1989 May;83(5):1676-81. (PMID: 2523415) ; J Exp Med. 1990 Jul 1;172(1):19-25. (PMID: 2141627) ; J Clin Invest. 1992 Apr;89(4):1274-81. (PMID: 1532589) ; J Clin Invest. 1995 Jun;95(6):2877-85. (PMID: 7769129) ; BMC Immunol. 2015 Mar 26;16:14. (PMID: 25887595) ; PLoS One. 2012;7(9):e46197. (PMID: 23049979) ; Am J Trop Med Hyg. 1999 Dec;61(6):932-40. (PMID: 10674673) ; Blood. 2003 Dec 15;102(13):4424-30. (PMID: 12855589) ; J Med Genet. 2010 Jul;47(7):471-5. (PMID: 19965803) ; Infect Immun. 2004 Oct;72(10):5630-7. (PMID: 15385460) ; Immunogenetics. 1998 Aug;48(3):222-32. (PMID: 9683667) ; Infect Immun. 2012 Dec;80(12):4435-43. (PMID: 23045477) ; Am J Trop Med Hyg. 1999 May;60(5):733-7. (PMID: 10344643) Grant Information: D43 TW005884 United States TW FIC NIH HHS; R01 AI051305 United States AI NIAID NIH HHS Contributed Indexing: Keywords: FcγRs; Malaria anemia; Polymorphisms; Susceptibility Substance Nomenclature: 0 (FCGR3A protein, human) ; 0 (FCGR3B protein, human) ; 0 (Fc gamma receptor IIA) ; 0 (GPI-Linked Proteins) ; 0 (Receptors, IgG) Entry Date(s): Date Created: 20170422 Date Completed: 20170807 Latest Revision: 20181202 Update Code: 20231215 PubMed Central ID: PMC5397742

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Association between Fcγ receptor IIA, IIIA and IIIB genetic polymorphisms and susceptibility to severe malaria anemia in children in western Kenya.