Abstract
Repeated infections by Plasmodium falciparum result in a humoral response that could reduce disease symptoms and prevent the development of clinical malaria. The principal mechanism underlying this humoral response is that immunoglobulin G (IgG) binds directly to the parasites, thus causing their neutralization. However, the action of antibodies alone is not always sufficient to eliminate pathogens from an organism. One key element involved in the recognition of IgG that plays a crucial role in the destruction of the parasites responsible for spreading malaria is the family of Fc gamma receptors. These receptors are expressed on the surface of immune cells. Several polymorphisms have been detected in the genes encoding these receptors, associated with susceptibility or resistance to malaria in different populations. In this review, we describe identified polymorphisms within the family of Fc gamma receptors and the impact of these variations on the response of a host to infection as well as provide new perspectives for the design of an effective vaccine for malaria.
Highlights
Despite the progress made against malaria, this disease remains a major public health concern, in sub-Saharan Africa [1]
This allele in homozygotes is associated with hemolytic anemia as well as unpredictable episodes of pain and generalized organ damage, all of which could be life-threatening for the carrier, it does appear in heterozygous individuals to be associated with a 90% greater chance of not developing severe malaria [6]
The simplest approach uses the polymerase chain reaction (PCR) in combination with restriction enzyme digestion; this process is known as allelespecific restriction enzyme digestion (ASRED) and is able to differentiate alleles and single nucleotide polymorphisms (SNPs) or single nucleotide variants (SNVs)
Summary
Despite the progress made against malaria, this disease remains a major public health concern, in sub-Saharan Africa (sSA) [1]. A binding comparable to that formed between two ITIM motifs and SHP1 is obtained— causing Lyn phosphorylation of tyrosine at position 536 and regulating SHP-1 phosphatase and inhibiting cell activation [36] This particular inhibition of ITAM-like receptors would have as an effect reduction of inflammation in animals and would serve as a basic mechanism for controlling the activation of both FcgRIIA and FcgRIIIA receptors [35, 37]. This receptor is highly expressed in B cells and can inhibit the activation of signals induced by B-cell receptors (BCRs) and regulate their effects [38] During this process, the ITIM motif, characterized by the presence of a single tyrosine, is phosphorylated by the protein tyrosine kinase (PTK) Src which allows the recruitment of the two SH2 domains from the proteins inositol phosphatase 1 and 2 (SHIP-1 and SHIP-2) [27]. The authors mentioned that “inside-out control’’ of Fcg receptors could be achieved by receptors others than Fcg receptors (toll-like receptor, cytokine/chemokine receptors, glucan receptors) [49,50,51]
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