Type 1 Innate Lymphoid Cells Regulate the Early Stage of Toxoplasma Gondii-Induced Neuroinflammation

2021 ◽  
Author(s):  
Johannes Steffen ◽  
Stefanie Ehrentraut ◽  
Ute Bank ◽  
Aindrila Biswas ◽  
Caio Andreeta Figueiredo ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
Early Stage ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells

scholarly journals Transcriptional regulatory networks that promote and restrict identities and functions of intestinal innate lymphoid cells

2018 ◽  
Author(s):  
Maria Pokrovskii ◽  
Jason A. Hall ◽  
David E. Ochayon ◽  
Ren Yi ◽  
Natalia S. Chaimowitz ◽  
...  
Keyword(s):  
Regulatory Networks ◽  
Inflammatory Diseases ◽  
Innate Lymphoid Cells ◽  
Chromatin Accessibility ◽  
Immune Defense ◽  
Lymphoid Cells ◽  
Transcriptional Regulatory Networks ◽  
Transcriptional Regulatory

SummaryInnate lymphoid cells (ILCs) can be subdivided into several distinct cytokine-secreting lineages that promote tissue homeostasis and immune defense but also contribute to inflammatory diseases. Accumulating evidence suggests that ILCs, similarly to other immune populations, are capable of phenotypic and functional plasticity in response to infectious or environmental stimuli. Yet the transcriptional circuits that control ILC identity and function are largely unknown. Here we integrate gene expression and chromatin accessibility data to infer transcriptional regulatory networks within intestinal type 1, 2, and 3 ILCs. We predict the “core” sets of transcription-factor (TF) regulators driving each ILC subset identity, among which only a few TFs were previously known. To assist in the interpretation of these networks, TFs were organized into cooperative clusters, or modules that control gene programs with distinct functions. The ILC network reveals extensive alternative-lineage-gene repression, whose regulation may explain reported plasticity between ILC subsets. We validate new roles for c-MAF and BCL6 as regulators affecting the type 1 and type 3 ILC lineages. Manipulation of TF pathways identified here might provide a novel means to selectively regulate ILC effector functions to alleviate inflammatory disease or enhance host tolerance to pathogenic microbes or noxious stimuli. Our results will enable further exploration of ILC biology, while our network approach will be broadly applicable to identifying key cell state regulators in otherin vivocell populations.

Type 1 innate lymphoid cells are associated with type 2 diabetes

2019 ◽  
Vol 45 (4) ◽  
pp. 341-346 ◽  
Author(s):  
F. Liu ◽  
H. Wang ◽  
W. Feng ◽  
X. Ye ◽  
X. Sun ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells

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 Microbiota instruct IL-17A-producing innate lymphoid cells to promote skin inflammation in cutaneous leishmaniasis

2021 ◽  
Author(s):  
Tej Pratap Singh ◽  
Augusto Carvalho ◽  
Elizabeth Grice ◽  
Phillip Scott
Keyword(s):  
Cutaneous Leishmaniasis ◽  
Staphylococcus Epidermidis ◽  
Leishmania Major ◽  
Inflammatory Responses ◽  
Skin Inflammation ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Skin Microbiota ◽  
Infected Skin

p.p1 {margin: 0.0px 0.0px 0.0px 0.0px; font: 12.0px Helvetica} span.s1 {color: #222222} span.s2 {font: 8.0px Helvetica} Innate lymphoid cells (ILCs) comprise a heterogeneous population of immune cells that maintain barrier function and can initiate a protective or pathological immune response upon infection. Here we show the involvement of IL-17A-producing ILCs in microbiota-driven immunopathology in cutaneous leishmaniasis. IL-17A-producing ILCs were RORgt + and were enriched in Leishmania major infected skin, and topical colonization with Staphylococcus epidermidis before L. major infection exacerbated the skin inflammatory responses and IL-17A-producing RORgt + ILC accumulation without impacting type 1 immune responses. IL-17A responses in ILCs were directed by Batf3 dependent CD103 + dendritic cells, and experiments using ILC deficient Rag1 -/- mice established that IL-17A + ILCs were sufficient in driving the inflammatory responses. As depletion of ILCs or neutralization of IL-17A diminished the microbiota mediated immunopathology. Taken together, this study indicates that the skin microbiota promotes RORgt + IL-17A-producing ILCs, which augment the skin inflammation in cutaneous leishmaniasis.

scholarly journals Group 2 Innate Lymphoid Cells (ILC2) Suppress Beneficial Type 1 Immune Responses During Pulmonary Cryptococcosis

2020 ◽  
Vol 11 ◽  
Author(s):  
Markus Kindermann ◽  
Lisa Knipfer ◽  
Stephanie Obermeyer ◽  
Uwe Müller ◽  
Gottfried Alber ◽  
...  
Keyword(s):  
Immune Responses ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Pulmonary Cryptococcosis ◽  
Group 2

scholarly journals An Overview of the Role of Innate Lymphoid Cells in Gut Infections and Inflammation

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Silvia Sedda ◽  
Irene Marafini ◽  
Michele M. Figliuzzi ◽  
Francesco Pallone ◽  
Giovanni Monteleone
Keyword(s):  
Transcription Factor ◽  
Decisive Role ◽  
Innate Lymphoid Cells ◽  
Small Population ◽  
Lymphoid Cells ◽  
Antigen Receptors ◽  
Immune Mediated ◽  
Lymphoid Organogenesis

Innate lymphoid cells (ILCs) are a group of hematopoietic cells devoid of antigen receptors that have important functions in lymphoid organogenesis, in the defense against extracellular pathogens, and in the maintenance of the epithelial barrier. Three distinct groups of ILCs have been identified on the basis of phenotypic and functional criteria and termed ILCs1, ILCs2, and ILCs3. Specifically, ILCs1 express the transcription factor T-bet and secrete T helper type-1- (Th1-) related cytokines, ILCs2 are dependent on the transcription factor RORαand express Gata-3 and the chemokine receptor homologous molecule (CRTH2) and produce Th2-related cytokines, and ILCs3 express the transcription factor RORγt and synthesize interleukin- (IL-) 17, IL-22, and, under specific stimuli, interferon-γ. ILCs represent a relatively small population in the gut, but accumulating evidence suggests that these cells could play a decisive role in orchestrating both protective and detrimental immune responses. In this review, we will summarize the present knowledge on the distribution of ILCs in the intestinal mucosa, with particular focus on their role in the control of both infections and effector cytokine response in immune-mediated pathologies.

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