scholarly journals HIV-1-induced cytokines deplete homeostatic innate lymphoid cells and expand TCF7-dependent memory NK cells

2020 ◽  
Vol 21 (3) ◽  
pp. 274-286 ◽  
Author(s):  
Yetao Wang ◽  
Lawrence Lifshitz ◽  
Kyle Gellatly ◽  
Carol L. Vinton ◽  
Kathleen Busman-Sahay ◽  
...  
Keyword(s):  
Nk Cells ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Hiv 1 ◽  
Memory Nk Cells

scholarly journals HIV-1-induced cytokines deplete homeostatic ILCs and expand TCF7-dependent memory NK cells: Supplemental Figures and Tables

2017 ◽  
Author(s):  
Yetao Wang ◽  
Kyle Gellatly ◽  
Sean McCauley ◽  
Pranitha Vangala ◽  
Kyusik Kim ◽  
...  
Keyword(s):  
Nk Cells ◽  
Inflammatory Cytokines ◽  
Nk Cell ◽  
Ex Vivo ◽  
Developmental Trajectory ◽  
Lymphoid Cells ◽  
Infected People ◽  
Cell Induction ◽  
Hiv 1 ◽  
Memory Nk Cells

HIV-1-infected people who take medications that suppress viremia, preserve CD4+ T cells, and prevent AIDS, have chronic inflammation with increased cardiovascular mortality. To investigate the etiology of this inflammation, the effect of HIV-1 on innate lymphoid cells (ILCs) and NK cells was examined. Homeostatic ILCs in blood and intestine were depleted permanently. NK cells were skewed towards a memory subset. Cytokines that are elevated during HIV-1 infection reproduced both abnormalities ex vivo. Pseudotime analysis of single NK cell transcriptomes revealed a developmental trajectory towards a subset with expression profile, chromatin state, and biological function like memory T lymphocytes. Expression of TCF7, a WNT transcription factor, increased over the course of the trajectory. TCF7 disruption, or WNT inhibition, prevented memory NK cell induction by inflammatory cytokines. These results demonstrate that inflammatory cytokines associated with HIV-1 infection irreversibly disrupt homeostatic ILCs and cause developmental shift towards TCF7+ memory NK cells.

scholarly journals The role of donor‐unrestricted T‐cells, innate lymphoid cells, and NK cells in anti‐mycobacterial immunity

2021 ◽  
Author(s):  
Paula Ruibal ◽  
Linda Voogd ◽  
Simone A. Joosten ◽  
Tom H. M. Ottenhoff
Keyword(s):  
T Cells ◽  
Nk Cells ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells

scholarly journals NK Cells Alleviate Lung Inflammation by Negatively Regulating Group 2 Innate Lymphoid Cells

2017 ◽  
Vol 198 (8) ◽  
pp. 3336-3344 ◽  
Author(s):  
Jiacheng Bi ◽  
Lulu Cui ◽  
Guang Yu ◽  
Xiaolu Yang ◽  
Youhai Chen ◽  
...  
Keyword(s):  
Nk Cells ◽  
Lung Inflammation ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Group 2

Tumor immunoevasion by the conversion of effector NK cells into type 1 innate lymphoid cells

2017 ◽  
Vol 18 (9) ◽  
pp. 1004-1015 ◽  
Author(s):  
Yulong Gao ◽  
Fernando Souza-Fonseca-Guimaraes ◽  
Tobias Bald ◽  
Susanna S Ng ◽  
Arabella Young ◽  
...  
Keyword(s):  
Nk Cells ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells

scholarly journals Toxoplasma gondiiInfection Drives Conversion of NK Cells into ILC1s

2019 ◽  
Author(s):  
Eugene Park ◽  
Swapneel J. Patel ◽  
Qiuling Wang ◽  
Prabhakar S. Andhey ◽  
Konstantin Zaitsev ◽  
...  
Keyword(s):  
Steady State ◽  
Tumor Microenvironment ◽  
Toxoplasma Gondii ◽  
Nk Cells ◽  
Natural Killer ◽  
Nk Cell ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Cell Conversion ◽  
Ongoing Infection

AbstractInnate lymphoid cells (ILCs) were originally classified based on their cytokine profiles, placing natural killer (NK) cells and ILC1s together, but recent studies support their separation into different lineages at steady-state. However, tumors may induce NK cell conversion into ILC1-like cells that are limited to the tumor microenvironment and whether this conversion occurs beyond this environment remains unknown. Here we describeToxoplasma gondiiinfection converts NK cells into cells resembling steady-state ILC1s that are heterogeneous and distinct from both steady-state NK cells and ILC1s in uninfected mice. Most toxoplasma-induced ILC1s were Eomes-dependent, indicating that NK cells can give rise to Eomes−Tbet-dependent ILC1-like cells that circulate widely and persist independent of ongoing infection. Moreover, these changes appear permanent, as supported by epigenetic analyses. Thus, these studies markedly expand current concepts of NK cells, ILCs, and their potential conversion.

scholarly journals Molecular definition of group 1 innate lymphoid cells in the mouse uterus

2018 ◽  
Author(s):  
Iva Filipovic ◽  
Laura Chiossone ◽  
Paola Vacca ◽  
Russell S Hamilton ◽  
Tiziano Ingegnere ◽  
...  
Keyword(s):  
Nk Cells ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Memory Cells ◽  
Mouse Uterus ◽  
Protein Ubiquitination ◽  
Reproductive Life ◽  
Definition Of ◽  
Molecular Patterns ◽  
Group 1

ABSTRACTDetermining the function of uterine lymphocytes is challenging because of the rapidly changing nature of the organ in response to sex hormones and, during pregnancy, to the invading fetal trophoblast cells. Here we provide the first genome-wide transcriptome atlas of mouse uterine group 1 innate lymphoid cells (g1 ILCs) at mid-gestation. The composition of g1 ILCs fluctuates throughout reproductive life, with Eomes-veCD49a+ ILC1s dominating before puberty and specifically expanding in second pregnancies, when the expression of CXCR6, a marker of memory cells, is upregulated. Tissue-resident Eomes+CD49a+ NK cells (trNK), which resemble human uterine NK cells, are most abundant during early pregnancy, and showcase gene signatures of responsiveness to TGF-β, connections with trophoblast, epithelial, endothelial and smooth muscle cells, leucocytes, as well as extracellular matrix. Unexpectedly, trNK cells express genes involved in anaerobic glycolysis, lipid metabolism, iron transport, protein ubiquitination, and recognition of microbial molecular patterns. Conventional NK cells expand late in gestation and may engage in crosstalk with trNK cells involving IL-18 and IFN-γ. These results identify trNK cells as the cellular hub of uterine g1 ILCs at mid-gestation and mark CXCR6+ ILC1s as potential memory cells of pregnancy.

scholarly journals Conventional NK cells and tissue-resident ILC1s join forces to control liver metastasis

2020 ◽  
Author(s):  
Laura Ducimetière ◽  
Giulia Lucchiari ◽  
Gioana Litscher ◽  
Marc Nater ◽  
Laura Heeb ◽  
...  
Keyword(s):  
Liver Metastasis ◽  
Nk Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Great Promise ◽  
Type I ◽  
Metastatic Niche

SUMMARYThe liver is a major metastatic target organ, and little is known about the role of immunity in controlling hepatic metastases. Here, we discovered that the concerted and non-redundant action of two innate lymphocyte subpopulations, conventional NK cells (cNKs) and tissue-resident type I Innate Lymphoid Cells (trILC1s), is essential for anti-metastatic defense. Using different preclinical models for liver metastasis, we found that trILC1 control metastatic seeding, whereas cNKs restrain outgrowth. The antimetastatic activity of cNKs is regulated in a tumor type-specific fashion. Thereby, individual cancer cell lines orchestrate the emergence of cNK subsets with unique phenotypic and functional traits. Understanding cancer-cell- as well as innate-cell-intrinsic factors will allow the exploitation of hepatic innate cells for development of novel cancer therapies.SignificanceInnate lymphoid cells hold great promise for the treatment of metastases. Development of effective therapies based on these versatile immune cells, however, is hampered by our limited knowledge of their behavior in the metastatic niche. Here, we describe that defense against liver metastasis requires the collaboration between two innate lymphocyte subsets, conventional NK cells (cNKs) and tissue-resident type I innate lymphoid cells (trILC1s). We show that different cancers generate their own particular metastatic niche inducing specific changes in cNKs and trILC1s. Further, we uncover specific cNK subsets that can be manipulated to improve their anti-metastatic potential. Our work contributes to understanding how cancer-specific factors and hepatic innate lymphocytes exert mutual influence and how this can be exploited for therapeutic purposes.HighlightscNKs and trILC1s collaborate to control hepatic metastasistrILC1s restrict seeding and cNKs control outgrowth of cancer cells in the liverIndividual cancer cell lines orchestrate a distinct metastatic nicheThe metastatic niche dictates the phenotype and function of cNKs

scholarly journals Innate Lymphoid Cells in Human Pregnancy

2020 ◽  
Vol 11 ◽  
Author(s):  
João Mendes ◽  
Ana Luísa Areia ◽  
Paulo Rodrigues-Santos ◽  
Manuel Santos-Rosa ◽  
Anabela Mota-Pinto
Keyword(s):  
Nk Cells ◽  
Innate Lymphoid Cells ◽  
Adverse Outcomes ◽  
Lymphoid Cells ◽  
Perinatal Medicine ◽  
Effector Cells ◽  
Human Pregnancy ◽  
Group 3 ◽  
Group 2 ◽  
In Pregnancy

Innate lymphoid cells (ILCs) are a new set of cells considered to be a part of the innate immune system. ILCs are classified into five subsets (according to their transcription factors and cytokine profile) as natural killer cells (NK cells), group 1 ILCs, group 2 ILCs, group 3 ILCs, and lymphoid tissue inducers (LTi). Functionally, these cells resemble the T helper population but lack the expression of recombinant genes, which is essential for the formation of T cell receptors. In this work, the authors address the distinction between peripheral and decidual NK cells, highlighting their diversity in ILC biology and its relevance to human pregnancy. ILCs are effector cells that are important in promoting immunity, inflammation, and tissue repair. Recent studies have directed their attention to ILC actions in pregnancy. Dysregulation or expansion of pro-inflammatory ILC populations as well as abnormal tolerogenic responses may directly interfere with pregnancy, ultimately resulting in pregnancy loss or adverse outcomes. In this review, we characterize these cells, considering recent findings and addressing knowledge gaps in perinatal medicine in the context of ILC biology. Moreover, we discuss the relevance of these cells not only to the process of immune tolerance, but also in disease.

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