Abstract
Although the KIR gene content polymorphism has been studied worldwide, only a few isolated or Amerindian populations have been analyzed. This extremely diverse gene family codifies receptors that are expressed mainly in NK cells and bind HLA class I molecules. KIR-HLA combinations have been associated to several diseases and population studies are important to comprehend their evolution and their role in immunity. Here we analyzed, by PCR-SSP (specific sequencing priming), 327 individuals from four isolated groups of two of the most important Brazilian Amerindian populations: Kaingang and Guarani. The pattern of KIR diversity among these and other ten Amerindian populations disclosed a wide range of variation for both KIR haplotypes and gene frequencies, indicating that demographic factors, such as bottleneck and founder effects, were the most important evolutionary factors in shaping the KIR polymorphism in these populations.
Highlights
Killer cell immunoglobulin-like receptors (KIR) are expressed on natural killer (NK) cells and subsets of T cells playing an important role in innate immunity and influencing the course of adaptive immune responses
HLA-B epitopes are currently considered the most important KIR3DL1/S1 ligands, we recently suggested that both HLA-A and B allotypes may be important for NK function [11], which corroborates the suggestion about HLAA and HLA-B having compensatory function in the engagement of KIR receptors and being a KIR-driven functional genetic block [12]
Gene Frequencies Comparing gene frequencies among populations, especially genetically isolated groups, is a powerful tool to understand the possible causes of variations in a certain gene or gene family and it may help to trace the history of the populations
Summary
Killer cell immunoglobulin-like receptors (KIR) are expressed on natural killer (NK) cells and subsets of T cells playing an important role in innate immunity and influencing the course of adaptive immune responses. These cells are regulated by many activating and inhibitory signals, including signals delivered by the interaction between KIR and their ligands [1]. KIR are encoded by genes in the 19q13.4 genomic region [2] and classified according to the number of extracellular Ig-like domains as KIR2D or KIR3D and according to the cytoplasmic tail as L (long) or S (short) [3] These structural features correlate with broad functional differences and with the characteristics of cognate ligands. The exception is KIR2DL4 that has the ability to transduce both activating and inhibitory signals [4]
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