Malaria-driven expansion of adaptive-like functional CD56-negative NK cells correlates with clinical immunity to malaria
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ABSTRACT:
PROVIDER: PRJNA868350 | ENA |
REPOSITORIES: ENA
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Project description:Natural Killer (NK) cells likely play an important role in immunity to malaria, but whether repeated malaria modifies the NK cell response remains unclear. Here, we comprehensively profiled the NK cell response in a cohort of 264 Ugandan children. Repeated malaria exposure was associated with expansion of an atypical, CD56neg population of NK cells that differed transcriptionally, epigenetically, and phenotypically from CD56dim NK cells, including decreased expression of PLZF and the Fc receptor g chain, increased histone methylation, and increased protein expression of LAG-3, KIR and LILRB1. CD56neg NK cells were highly functional, displaying greater antibody dependent cellular cytotoxicity than CD56dim NK cells, and higher frequencies of these cells were associated with protection against symptomatic malaria and high parasite densities. Importantly, following marked reductions in malaria transmission, frequencies of these cells rapidly declined, suggesting that continuous exposure to malaria is required to maintain this modified, adaptive-like NK cell subset.
2022-12-25 | GSE210943 | GEO
Project description:A small subset of T cells also expresses kiler-cell immunoglobulin-like receptors (KIRs). We find that KIR+ T cells primarily reside in the CD56+ T population. However, little is known on how these cells are different from the conventional CD56- T, NK, and iNKT cells. We used microarray profiling to compare and determine the distinctive differences of CD56+ T cell and its KIR subsets when compared to the conventional CD56- T, NK and iNKT cells. Lymphocyte subsets were sorted from human peripheral blood mononuclear cells with FACSAriaII (BD Biosciences, San Jose, CA) using anti-CD3, anti-CD56, anti-CD14, anti-KIR2DL1, anti-KIR2DL2/3, anti-KIR3DL1 and anti-TCRValpha24 antibodies. The purity of CD3+CD56- T cells, CD3-CD56+ NK cells, CD3+CD56+ T cells, KIR-CD3+CD56+ T cells, and KIR+CD3+CD56+ T cells were more than 98% in all experiments. The purities of iNKT cells for TCRValpha24 and CD1d-tetramer were >95% and >90%, respectively. RNA pre-amplification, labeling and hybridization on Human Genome U133Plus 2.0 GeneChip array were performed in the St. Jude Hartwell Center for Bioinformatics & Biotechnology microarray core facility according to the manufacturer’s instructions (Affymetrix, Santa Clara, CA).
2013-07-01 | E-GEOD-47855 | biostudies-arrayexpress
Project description:A small subset of T cells also expresses kiler-cell immunoglobulin-like receptors (KIRs). We find that KIR+ T cells primarily reside in the CD56+ T population. However, little is known on how these cells are different from the conventional CD56- T, NK, and iNKT cells. We used microarray profiling to compare and determine the distinctive differences of CD56+ T cell and its KIR subsets when compared to the conventional CD56- T, NK and iNKT cells.
2013-07-01 | GSE47855 | GEO
Project description:Pooled purified peripheral blood derived CD56dimCD16+ NK, CD56brightCD16- NK and in vitro activated CD56+CD16+ NK subsets obtained from 9 healthy donors were analyzed for gene expression pattern. Each pooled NK subset sample was hybridized in replicates (A and B). Keywords: other
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Project description:In order to gain a better understanding of gene expression during early malaria infection, we conducted microarray analysis of early blood responses in mice infected with erythrocytic stage Plasmodium chabaudi. Immediately following infection, we observed coordinated and sequential waves of immune responses, with interferon-associated gene transcripts dominating by 16 hours post-infection, followed by strong increases in natural killer (NK) cell-associated and MHC class I-related transcripts by 32 hours post-infection. We hypothesized that the observed elevation in NK cell-associated transcripts could be the result of a dramatic increase in the proportion of NK cells in the blood during infection, which we confirmed by flow cytometry. Subsequent microarray analysis of NK cells isolated from the peripheral blood of infected mice revealed a cell proliferation expression signature consistent with the observation that NK cells replicate in response to infection. Early proliferation of NK cells was directly observed in studies with adoptively transferred cells in infected mice. These data indicate that the early response to P. chabaudi infection of the blood is marked by a primary wave of interferon with a subsequent response by NK cells. Keywords: murine NK cell response to Plasmodium chabaudi infection We analyzed a series of 10 MEEBO arrays on which were hybed RNA amplified from NK cells of C57BL/6 mice either mock-infected or infected with P. chabaudi AS.
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Project description:In order to gain a better understanding of gene expression during early malaria infection, we conducted microarray analysis of early blood responses in mice infected with erythrocytic stage Plasmodium chabaudi. Immediately following infection, we observed coordinated and sequential waves of immune responses, with interferon-associated gene transcripts dominating by 16 hours post-infection, followed by strong increases in natural killer (NK) cell-associated and MHC class I-related transcripts by 32 hours post-infection. We hypothesized that the observed elevation in NK cell-associated transcripts could be the result of a dramatic increase in the proportion of NK cells in the blood during infection, which we confirmed by flow cytometry. Subsequent microarray analysis of NK cells isolated from the peripheral blood of infected mice revealed a cell proliferation expression signature consistent with the observation that NK cells replicate in response to infection. Early proliferation of NK cells was directly observed in studies with adoptively transferred cells in infected mice. These data indicate that the early response to P. chabaudi infection of the blood is marked by a primary wave of interferon with a subsequent response by NK cells. Keywords: murine NK cell response to Plasmodium chabaudi infection
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Project description:The innate cytotoxic Natural Killer (NK) cells emerged during hematopoiesis through a linear model of human NK development, yet how in vitro model of NK differentiation recapitulates in vivo process is largely under-explored. Here, we established that NK cell trajectory in vitro can be divided into 4 stages by sequential acquisition of CD161, CD56 and CD94 in which CD56 bifurcation can separate Stage 3a (CD56-) as ILC-precursor that can further give rise to stage 3b (CD56+) and stage 4 (CD94+). Re-plating results together with clonal tracing between S3b, S4 and ILC3 subsets supported a diverging developmental point between NK and ILC3 lineages occurs at the S3a stage and accompanied by the loss of the ILC3 potential as NK cell maturation progress from S3b toward S4. Single-cell transcriptomic and RNA-velocity connected the NK cytotoxic trajectory with a coordinated network of transcription factors (TFs) that are highly compatible with primary NK cell gene program.
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Project description:There is limited knowledge on the origin and development of the ample spectrum of human NK cells, particularly of specialized NK subsets. Here, we characterized the NK cell progeny of CD34+DNAM-1bright CXCR4+ precursors that reside in healthy bone marrow and circulate in the peripheral blood (PB) of patients with chronic infections/inflammation. including HIV, HCV or HCMV reactivation after HSC transplantation. Unlike conventional CD34+ precursors they rapidly differentiated in vitro into cytotoxic, IFNγ-secreting CD94/NKG2C+KIR+CD57+ maturing NK cell progenies with HCMV-inhibiting activity. Progeny characterization led also to identification of an additional new PB Lin-CD56-CD16+ precursor giving rise to the same CD94/NKG2C+KIR+CD57+ maturing NK cell progenies. Microarray analysis of NK cell progenies revealed a signature compatible with maturing adaptive NK cells. In vivo circulation of multiple common lymphocyte precursors with rapid development to NKG2C+ NK cell progeny is steadily occurring and may thus be a crucial resource for the prompt control of HCMV. We used microarray to compare the transcriptional profiles of human NKG2C+ NK cells derived from i) CD34+DNAM1brightCXCR4+ precursors, ii) Lin-CD34-CD16+CD56- precursors, iii) peripheral blood.
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Project description:In order to gain a better understanding of gene expression during early malaria infection, we conducted microarray analysis of early blood responses in mice infected with erythrocytic stage Plasmodium chabaudi. Immediately following infection, we observed coordinated and sequential waves of immune responses, with interferon-associated gene transcripts dominating by 16 hours post-infection, followed by strong increases in natural killer (NK) cell-associated and MHC class I-related transcripts by 32 hours post-infection. We hypothesized that the observed elevation in NK cell-associated transcripts could be the result of a dramatic increase in the proportion of NK cells in the blood during infection, which we confirmed by flow cytometry. Subsequent microarray analysis of NK cells isolated from the peripheral blood of infected mice revealed a cell proliferation expression signature consistent with the observation that NK cells replicate in response to infection. Early proliferation of NK cells was directly observed in studies with adoptively transferred cells in infected mice. These data indicate that the early response to P. chabaudi infection of the blood is marked by a primary wave of interferon with a subsequent response by NK cells. Keywords: murine whole blood response to Plasmodium chabaudi infection We analyzed a series of 36 MEEBO arrays on which were hybed RNA amplified from whole blood of C57BL/6 mice either mock-infected or infected with P. chabaudi AS.
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