Immune modules shared by innate lymphoid cells and T cells

Robinette, Michelle L.; Colonna, Marco

doi:10.1016/j.jaci.2016.09.006

Cited by 66 publications

(62 citation statements)

References 125 publications

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“…In the modern paradigm that NK cells mirror CD8 + T cells, while ILCs parallel CD4 + T cells3, it is worthwhile to consider the γ c requirements of T cells. All naïve T cells predominantly utilize T cell receptor (TCR) signalling and IL-7 for their survival83948.…”

Section: Discussionmentioning

confidence: 99%

“…Innate lymphoid cells (ILC) are a lineage of professional cytokine-producing cells that mirror T cells in transcriptional circuitry and effector functions, but derive from distinct progenitors and do not express recombined antigen-specific receptors123. Primary ILC classes encompass natural killer (NK) cells, which parallel cytotoxic CD8 + T cells, and three additional groups of ILCs enriched at mucosal surfaces that mirror polarized CD4 + helper T cell subsets, called ILC1, ILC2, and ILC3 (refs 1, 2, 3).…”

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confidence: 99%

“…Primary ILC classes encompass natural killer (NK) cells, which parallel cytotoxic CD8 + T cells, and three additional groups of ILCs enriched at mucosal surfaces that mirror polarized CD4 + helper T cell subsets, called ILC1, ILC2, and ILC3 (refs 1, 2, 3). Functionally, Eomes − T-bet + ILC1, like Eomes + T-bet + NK cells, produce IFN-γ, whereas GATA3 + ILC2 produce IL-5 and IL-13, and RORγt + ILC3 produce IL-22 and/or IL-17.…”

mentioning

confidence: 99%

“…Functionally, Eomes − T-bet + ILC1, like Eomes + T-bet + NK cells, produce IFN-γ, whereas GATA3 + ILC2 produce IL-5 and IL-13, and RORγt + ILC3 produce IL-22 and/or IL-17. In mouse, ILC3 are a particularly diverse lineage, and include fetal lymphoid tissue inducer (LTi) cells, as well as three adult subsets, T-bet − CCR6 + LTi-like ILC3, T-bet lo CCR6 − NKp46 − (double negative, DN) ILC3, and T-bet + NKp46 + ILC3 (refs 2, 3). …”

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confidence: 99%

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IL-15 sustains IL-7R-independent ILC2 and ILC3 development

et al. 2017

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The signals that maintain tissue-resident innate lymphoid cells (ILC) in different microenvironments are incompletely understood. Here we show that IL-7 receptor (IL-7R) is not strictly required for the development of any ILC subset, as residual cells persist in the small intestinal lamina propria (siLP) of adult and neonatal Il7ra−/− mice. Il7ra−/− ILC2 primarily express an ST2− phenotype, but are not inflammatory ILC2. CCR6+ ILC3, which express higher Bcl-2 than other ILC3, are the most abundant subset in Il7ra−/− siLP. All ILC subsets are functionally competent in vitro, and are sufficient to provide enhanced protection to infection with C. rodentium. IL-15 equally sustains wild-type and Il7ra−/− ILC survival in vitro and compensates for IL-7R deficiency, as residual ILCs are depleted in mice lacking both molecules. Collectively, these data demonstrate that siLP ILCs are not completely IL-7R dependent, but can persist partially through IL-15 signalling.

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Section: Discussionmentioning

confidence: 99%

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IL-15 sustains IL-7R-independent ILC2 and ILC3 development

et al. 2017

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“…ILCs are lymphocyte-like cells, but lack markers of mature lymphocytes, and do not express allergen-specific T cell receptors. ILC2s are regarded as innate counterparts of Th2 cells because both share the same functional module by their mutual production of signature cytokines, such as IL-5 and IL-13 46. For example, GATA-3 is a key transcriptional factor that plays parallel roles in the development and function of both Th2 cells and ILC2s 47.…”

Section: Pathogenesis and Endotypes Of Crsmentioning

confidence: 99%

Emerging Endotypes of Chronic Rhinosinusitis and Its Application to Precision Medicine

Kim

Cho

2017

Allergy Asthma Immunol Res

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Chronic rhinosinusitis (CRS) is a heterogeneous inflammatory disease with various underlying pathophysiologic mechanisms which translate to endotypes, in contrast to clinical phenotypes or histological subtypes. Defining endotypes can help clinicians predict disease prognosis, select subjects suitable for a specific therapy, and assess risks for comorbid conditions, including asthma. Therefore, with recent advancement of biologicals in CRS clinical trials, endotyping can be a breakthrough in treating recalcitrant CRS. CRS is caused by dysregulated immunologic responses to external stimuli, which induce various inflammatory mediators from inflammatory cells, including innate lymphoid cells (ILCs) and T lymphocytes as well as epithelial cells. Thymic stromal lymphopoietin (TSLP), interleukin (IL)-25, and IL-33, which are mainly secreted by epithelial cells in response to external stimuli, act on type 2 ILCs and T helper 2 (Th2) cells, inducing IL-4, IL-5, and IL-13. Local immunoglobulin E (IgE) production is also a signature event in nasal polyps (NP). These inflammatory mediators are novel potential therapeutic targets for recalcitrant CRS. This article reviews recent publications regarding endotypes and endotype-based therapeutic strategies in CRS and NP.

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Phenotypes, roles, and modulation of regulatory lymphocytes in periodontitis and its associated systemic diseases

Zou

Zhou

Huang

et al. 2021

Journal of Leukocyte Biology

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Periodontitis is a common chronic inflammatory disease that can result in tooth loss and poses a risk to systemic health. Lymphocytes play important roles in periodontitis through multiple mechanisms. Regulatory lymphocytes including regulatory B cells (Bregs) and T cells (Tregs) are the main immunosuppressive cells that maintain immune homeostasis, and are critical to our understanding of the pathogenesis of periodontitis and the development of effective treatments. In this review, we discuss the phenotypes, roles, and modulating strategies of regulatory lymphocytes including Bregs and Tregs in periodontitis and frequently cooccurring inflammatory diseases such as rheumatoid arthritis, Alzheimer disease, diabetes mellitus, and stroke. The current evidence suggests that restoring immune balance through therapeutic targeting of regulatory lymphocytes is a promising strategy for the treatment of periodontitis and other systemic inflammatory diseases.

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Immune modules shared by innate lymphoid cells and T cells

Cited by 66 publications

References 125 publications

IL-15 sustains IL-7R-independent ILC2 and ILC3 development

IL-15 sustains IL-7R-independent ILC2 and ILC3 development

Emerging Endotypes of Chronic Rhinosinusitis and Its Application to Precision Medicine

Phenotypes, roles, and modulation of regulatory lymphocytes in periodontitis and its associated systemic diseases

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