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Immune Testing in Recurrent Pregnancy Loss*
Published in Howard J.A. Carp, Recurrent Pregnancy Loss, 2020
Jeffrey Braverman, Darren Ritsick, Nadera Mansouri-Attia
The number and identity of activating and inhibitory killer immune-like receptors (KIRs) expressed by uNK cells (categorized as KIR A and KIR B haplotypes) and the HLA-C allotypes expressed by uterine stromal cells determine the threshold for uNK cell activation which is critical for angiogenic cytokine secretion and spiral artery remodeling. Specific combinations of maternal KIR haplotypes, maternal HLA-C allotypes, and embryonic HLA-C allotypes have been found to inadequately activate uNK cell cytokine secretion and are associated with increased risk for poor placentation, which results in increased rates of spontaneous miscarriage and preeclampsia as well as low birth weight [15–18]. These combinations include maternal KIR haplotypes lacking activating KIRs (A haplotypes and B haplotypes lacking the KIR2DS1 gene), particularly when the embryonic HLA-C2 allele content is greater than the maternal HLA-C2 allele content (by virtue of a paternally-contributed C2 allele).
Disease-association of different killer cell immunoglobulin-like receptors (KIR) and HLA-C gene combinations in reactive arthritis
Published in Modern Rheumatology, 2019
Hong Sheng Sun, Dong Xia Liu, Yan Yan Bai, Nai Wen Hu
Holm et al. suggest that KIR2DS1 susceptibility can be linked to psoriatic arthritis and not to the psoriatic condition [49]. Other researchers found an association of the KIR2DS1 gene with HLA-Cw*0602 in psoriasis vulgaris patients [50]. Higher genotypic frequencies of KIR2DS1 and more frequent occurrences with two additional activating KIR genes were reported in SLE patients than in controls [35]. In our study, the increased frequencies of the KIR2DS1 and two activating KIR genes were observed in ReA patients compared with the controls. Fauriat et al. reported that KIR2DS1 reduces the responsiveness of NK cells to target cell recognition [51]. The increased frequency of the KIR2DS1 gene in ReA patients decreases NK cell cytotoxicity against target cells (e.g. infected cells and autoreactive T cells) and results in persistent infection and auto-antibody production.
Expression of HLA-G and KIR2DL4 receptor in chorionic villous in missed abortion
Published in Gynecological Endocrinology, 2020
Olesya Bespalova, Margarita Bakleicheva, Tatiana Ivashchenko, Tatiana Tral, Gulrukhsor Tolibova, Igor Kogan
Several genetic association studies point to a useful role for NK activation in early pregnancy and the presence of activating human killer cell immunoglobulin-like receptors (KIR) such as KIR2DS1 has been shown to favor reproductive success. In agreement with this, the production of proinflammatory cytokines in response to HLA-G has been detected in uterine NK cells isolated during the window of implantation and in the activated decidual NK cells from first-trimester abortions. Analysis of the transcriptional response to activation via KIR2DL4 revealed the up-regulation of a restricted set of chemokines and cytokines, including IFN-γ, TNF-α, IL-1β, IL-6, and IL-8 that can promote vascular remodeling directly or indirectly by acting on other cell types in the local environment.
Low number of KIR ligands in lymphoma patients favors a good rituximab-dependent NK cell response
Published in OncoImmunology, 2021
Dhon Roméo Makanga, Maxime Jullien, Gaëlle David, Nolwenn Legrand, Catherine Willem, Léa Dubreuil, Alexandre Walencik, Cyrille Touzeau, Thomas Gastinne, Benoit Tessoulin, Steven Le Gouill, Béatrice Mahé, Katia Gagne, Patrice Chevallier, Béatrice Clemenceau, Christelle Retière
Several mechanisms of cancer resistance to rituximab have been documented in the literature, and different strategies are used to increase the effector activity of NK cells to improve anti-tumor responses. The inhibition of the ADCC function of NK cells through interactions between inhibitory killer cell immunoglobulin-like receptors (KIRs) and HLA class I ligands has been described as one of the potential mechanisms of cancer resistance to rituximab8,9 . KIRs are mainly expressed by NK cells and modulate NK cell responses by recognizing HLA class I molecules in tumoral or virus-infected cells. The interactions between KIR and autologous HLA class I ligands during development contribute to the functional education of KIR+ NK cells.10 This functional competence gives educated KIR+ NK cells the ability to recognize and eliminate target cells that exhibit an absence of expression (missing-self) or a downregulation of HLA class I molecules. The main inhibitory KIRs are KIR2DL1, KIR2DL2/3 and KIR3DL1, which, respectively, recognize HLA-C molecules of group C2 (Lys80), HLA-C molecules of group C1 (Asn80) and Bw4 motifs bearing some HLA-A and HLA-B molecules. In contrast, the activating KIR2DS1 triggers NK cell alloreactivity by recognizing HLA-C molecules of group C2 on the surface of allogenic target cells only when KIR2DS1+ NK cells have evolved in a C2− environment.11–13 KIR genes are clonally expressed on the surface of NK cells.14 Thus, the KIR+ NK cell repertoire is diverse between individuals, since the NK cell repertoire harbors different NK cell populations with different functional orientations.