Expansion of the Knops blood group system and subdivision of Sl<sup>a</sup>

Moulds, Joann M.; Zimmerman, Peter A.; Doumbo, Ogobara K.; Diallo, Dapa A.; Atkinson, John P.; Krych-Goldberg, Malgorzata; Hourcade, Dennis E.

doi:10.1046/j.1537-2995.2002.00002.x

Cited by 32 publications

(33 citation statements)

References 18 publications

(18 reference statements)

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“…Several antigens have been described in the Knops blood group system on CR1; Knops antigens a and b (Kn a /Kn b ), rs41274768 [19], McCoy a and b (McC a /McC b ), rs17047660 [20], Swain-Langley 1 and 2 (Sl1/Sl2), rs17047661 [20,21], KCAM + and - (KCAM + /KCAM - ), rs6691117 [22], York + and - (Yka + /Yka - ), rs3737002 [23] and Sl3,rs4844609 [21]. …”

Section: Introductionmentioning

confidence: 99%

Human genetic polymorphisms in the Knops blood group are not associated with a protective advantage against Plasmodium falciparum malaria in Southern Ghana

Hansson

Kurtzhals

Goka

et al. 2013

Malar J

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BackgroundThe complex interactions between the human host and the Plasmodium falciparum parasite and the factors influencing severity of disease are still not fully understood. Human single nucleotide polymorphisms SNPs associated with Knops blood group system; carried by complement receptor 1 may be associated with the pathology of P. falciparum malaria, and susceptibility to disease.MethodsThe objective of this study was to determine the genotype and haplotype frequencies of the SNPs defining the Knops blood group antigens; Kna/b, McCoya/b, Swain-Langley1/2 and KCAM+/- in Ghanaian patients with malaria and determine possible associations between these polymorphisms and the severity of the disease. Study participants were patients (n = 267) admitted to the emergency room at the Department of Child Health, Korle-Bu Teaching Hospital, Accra, Ghana during the malaria season from June to August in 1995, 1996 and 1997, classified as uncomplicated malaria (n = 89), severe anaemia (n = 57) and cerebral malaria (n = 121) and controls who did not have a detectable Plasmodium infection or were symptomless carriers of the parasite (n = 275). The frequencies were determined using a post-PCR ligation detection reaction-fluorescent microsphere assay, developed to detect the SNPs defining the antigens. Chi-square/Fisher’s exact test and logistic regression models were used to analyse the data.ResultsAs expected, high frequencies of the alleles Kna, McCb, Sl2 and KCAM- were found in the Ghanaian population. Apart from small significant differences between the groups at the Sl locus, no significant allelic or genotypic differences were found between the controls and the disease groups or between the disease groups. The polymorphisms define eight different haplotypes H1(2.4%), H2(9.4%), H3(59.8%), H4(0%), H5(25.2%), H6(0.33%), H7(2.8%) and H8(0%). Investigating these haplotypes, no significant differences between any of the groups were found.ConclusionThe results confirm earlier findings of high frequencies of certain CR1 alleles in Africa; and shed more light on earlier conflicting findings; the alleles McCb, Sl2, Knb and KCAM- or combined haplotypes do not seem to confer any protective advantage against malaria infection or resulting disease severity. Based on these findings, in a very well-characterized population, malaria does not seem to be the selective force on these alleles.

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Section: Introductionmentioning

confidence: 99%

Human genetic polymorphisms in the Knops blood group are not associated with a protective advantage against Plasmodium falciparum malaria in Southern Ghana

Hansson

Kurtzhals

Goka

et al. 2013

Malar J

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“…72 A detailed characterization of the molecular basis of most of the Knops system antigens was performed by Moulds and coworkers. [73][74][75] The authors confirmed their data by performing inhibition studies with recombinant CR1 truncations. …”

Section: Cr1 Structure and Expression Patternmentioning

confidence: 53%

Development of complement therapeutics for inhibition of immune‐mediated red cell destruction

Yazdanbakhsh

2005

Transfusion

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A major objective of my National Blood Foundation (NBF)-funded proposal was to produce recombinant soluble forms of a complement regulatory protein called complement receptor 1 (CR1) that carries the Knops blood group system antigens to perform antibody neutralization studies. By generating these recombinant proteins, we were able to inhibit several Knops antibodies in patient serum samples, thereby demonstrating their usefulness for clinical use. Interestingly, the recombinant CR1 proteins generated through NBF funding were also found to strongly reduce complement-mediated red cell destruction in a mouse hemolytic transfusion model. In this review, I will outline our NBF-funded studies, give an overview of recent advances from our group and others in the development of complement therapeutics, and highlight their potential use in the transfusion medicine setting. THE COMPLEMENT SYSTEM IN TRANSFUSION MEDICINEThe complement system is an important part of the innate immune system that responds to challenges by microorganisms before an adaptive response has developed. 1 It is also an important regulator of B-cell, and possibly T-cell, immunity. 2 In addition to its essential role in immune defense, the complement system contributes to tissue damage in many clinical conditions, including ischemia-reperfusion injuries after myocardial infarction, and in patients undergoing cardiopulmonary bypass. 3,4 In the transfusion medicine setting, complement-mediated red cell (RBC) destruction plays a critical role, being involved in both intravascular and extravascular hemolysis. 5 Generally, in the presence of a potent, complement-binding antibody and large numbers of closely situated RBC antigens, complement activation can proceed to completion, resulting in intravascular hemolysis, which can be fatal. 6 The majority of blood group antibodies (including both allo-and autoantibodies) that can fix complement, however, only activate complement up to the C3 stage but do not go on to act as hemolysins. Although antibody-coated RBCs can be destroyed extravascularly without complement activation, RBC removal by tissue macrophages in the spleen and liver is enhanced considerably when C3 is present on RBCs in addition to immunoglobulin G (IgG). Indeed, as many as 50 percent of patients with autoimmune hemolytic anemia have both IgG and complement on their RBCs. 7Address reprint requests to: Karina Yazdanbakhsh, PhD, Complement Biology, New York Blood Center, 310, E 67th Street, New York, NY 10021; kyazdanbakhsh@nybloodcenter.org. HHS Public Access Author Manuscript Author ManuscriptAuthor Manuscript Author ManuscriptComplement-mediated intravascular and extravascular destruction of RBCs has been implicated as a contributing cause of anemia associated with sickle cell disease (SCD) [8][9][10][11][12][13][14][15][16][17][18] and in severe malarial infection. [19][20][21][22][23][24][25] In addition, in patients with paroxysmal nocturnal hemoglobinuria (PNH) syndrome, the observed intravascular hemolysis is due to increased sen...

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“…Another CR1 polymorphism of interest relates to the Knops blood group system. This system consists of nine antigens (KN1-KN9) comprising the three antigenic pairs V1561M, K1590E and R1601G and one conformational epitope (R1601 with S1610) in CCP25, and the single antigens T1408 located in the linker between CCPs 22-23 and I1615 in CCP25 (Table 2) (Covas et al, 2007;Moulds et al, 1991Moulds et al, , 2002Moulds et al, , 2005Veldhuisen et al, 2011).…”

Section: Complement Receptor 1 and Malariamentioning

confidence: 99%

More than just immune evasion: Hijacking complement by Plasmodium falciparum

Schmidt

Kennedy

Tham

2015

Molecular Immunology

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Expansion of the Knops blood group system and subdivision of Sl^a

Cited by 32 publications

References 18 publications

Human genetic polymorphisms in the Knops blood group are not associated with a protective advantage against Plasmodium falciparum malaria in Southern Ghana

Human genetic polymorphisms in the Knops blood group are not associated with a protective advantage against Plasmodium falciparum malaria in Southern Ghana

Development of complement therapeutics for inhibition of immune‐mediated red cell destruction

More than just immune evasion: Hijacking complement by Plasmodium falciparum

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Expansion of the Knops blood group system and subdivision of Sla

Cited by 32 publications

References 18 publications

Human genetic polymorphisms in the Knops blood group are not associated with a protective advantage against Plasmodium falciparum malaria in Southern Ghana

Human genetic polymorphisms in the Knops blood group are not associated with a protective advantage against Plasmodium falciparum malaria in Southern Ghana

Development of complement therapeutics for inhibition of immune‐mediated red cell destruction

More than just immune evasion: Hijacking complement by Plasmodium falciparum

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Product

Resources

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Expansion of the Knops blood group system and subdivision of Sl^a