IGHG3 G and the Pathogenesis of Hyperreactive malarious splenomegaly

Kelly, Kevin M.

doi:10.1016/s0306-9877(96)90013-4

Cited by 9 publications

(6 citation statements)

References 24 publications

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“…IgG3-containing complexes could mediate beneficial effects, such as Ab-dependent cellular cytotoxicity and phagocytosis of the parasite, or pathological inflammation. Kelly proposed the hypothesis that in a population with a high frequency of a mutant allotype of IgG3, a chronic presence of circulating immune complexes of unknown malaria antigens with IgG3 contributes to hyperreactive malarious splenomegaly, a chronic complication of malaria associated with up to 60% mortality (21). However, anti-Block 2 Abs, shown here to be mostly IgG3, are strongly associated with protection against clinical malaria, with protective efficacy in the range of 22 to 46% for typespecific Abs against types of Block 2 that are most prevalent in natural populations of P. falciparum (10).…”

mentioning

confidence: 99%

Differential Patterns of Human Immunoglobulin G Subclass Responses to Distinct Regions of a Single Protein, the Merozoite Surface Protein 1 ofPlasmodium falciparum

et al. 2001

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Comparisons of immunoglobulin G (IgG) subclass responses to the major polymorphic region and to a conserved region of MSP-1 in three cohorts of African villagers exposed to Plasmodium falciparum revealed that responses to Block 2 are predominantly IgG3 whereas antibodies to MSP-1 19 are mainly IgG1. The striking dominance of IgG3 to Block 2 may explain the short duration of this response and also the requirement for continuous stimulation by malaria infection to maintain clinical immunity.

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confidence: 99%

Differential Patterns of Human Immunoglobulin G Subclass Responses to Distinct Regions of a Single Protein, the Merozoite Surface Protein 1 ofPlasmodium falciparum

et al. 2001

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“…At the extreme end of the spectrum, patients can develop hyperreactive malarial splenomegaly, a syndrome of excessive immune response to malaria marked by extreme organ enlargement, high total IgM and elevated malaria antibody titres. Hyperreactive malarial splenomegaly has been associated with human leucocyte antigen (HLA)–DR2 and the immunoglobulin haplotype, IgHG3 (Kelly, ; Tano et al , ).…”

Section: P Falciparum Malariamentioning

confidence: 99%

“…HbF and HbA2) and genetic modifiers of malarial splenomegaly (e.g. HLA‐DR2 and IgHG3) should be investigated in SCD patients with splenomegaly (Bhatia & Crane, ; Kelly, ; Steinberg & Sebastiani, ). For example, the HLA‐DR2 phenotype is associated with hyperreactive splenomegaly (Bhatia & Crane, ) and protects against stroke in patients with SCD (Styles et al , ) but has not been defined in patients with both splenomegaly and SCD.…”

Section: The Spleen In Scd In Africa: What Is the Impact Of Malaria?mentioning

confidence: 99%

Turf wars: exploring splenomegaly in sickle cell disease in malaria‐endemic regions

Tubman

Makani

2017

Br J Haematol

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Summary Sickle cell disease (SCD) is a group of recessively inherited disorders of erythrocyte function that presents an ongoing threat to reducing childhood mortality around the world. While decades of research have led to improved survival for SCD patients in wealthy countries, survival remains dismal in low- and middle-income countries. Much of the early mortality associated with SCD is attributed to increased risk of infections due to early loss of splenic function. In the West, bacterial infections with encapsulated organisms are a primary concern. In sub-Saharan Africa, where the majority of infants with SCD are born, the same is true; however malaria presents an additional threat to survival. The search for factors that define variability in sickle cell phenotypes should include environmental modifiers, such as malaria. Further exploration of this relationship could lead to novel strategies to reduce morbidity and mortality attributable to infections. In this review, we explore the interactions between SCD, malaria and the spleen to better understand how splenomegaly and splenic (dys)function may co-exist in patients with SCD living in malaria-endemic areas.

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“…De même, une susceptibilité familiale a été rapportée dans une étude [32]. Les antigènes du complexe majeur d'histocompatibilité (notamment HLA DR2) semblent être impliqués au premier plan dans cette prédisposi-tion mais d'autres facteurs génétiques ont également été discutés (chaînes lourdes d'IgG [33], molécule CD1 [34]. .…”

Section: éLéments De Physiopathologieunclassified