Innate lymphoid cell regulation of adaptive immunity

Withers, David R.

doi:10.1111/imm.12639

Cited by 53 publications

(45 citation statements)

References 88 publications

(229 reference statements)

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“…Whilst these data conflict with previous reports on the requirement for ICOS-ICOSL in ILC2 homeostasis, this may reflect differences arising from the animal facility in which the studies were conducted. We decided to characterise ILC populations in CD80 -/- CD86 -/- mice since there is evidence to support ILC expression of CD28 and a block in T cell activation might reveal further insight into the effects of ILC:T cell cross talk 29 – 31 . It was noticeable that in the intestine, the ILC3 population was enhanced, which might reflect greater availability of cytokines such as IL-7 and IL-15, although the absence of T cell responses to the commensal microbial population is obviously a further potential factor.…”

Section: Discussionmentioning

confidence: 99%

Characterisation of innate lymphoid cell populations at different sites in mice with defective T cell immunity

Dutton¹,

Camelo²,

Sleeman³

et al. 2018

Wellcome Open Res

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Background: Innate lymphoid cells (ILCs) have now been identified within most tissues of the body and current evidence indicates that this family of cells play a fundamental role in maintaining tissue homeostasis. However, few studies have compared the ILC populations between several tissues. Methods: We sought to generate a comprehensive characterisation of the ILC populations in different tissues of C57BL/6 WT and genetically modified mice targeting costimulatory pathways, using transcription factor expression to define specific groups. Results: Consistent with studies individually describing the ILC composition in different tissues, our analysis revealed different ILC groups dominate the ILC population in different tissues. Additionally, we observed a population of IL-7Rα +Id2 + cells lacking expression of lineage markers but also lacking expression of GATA-3, RORgt or T-bet. This population was most evident in ear skin where it outnumbered the defined ILC groups, however, further experiments demonstrated that detection of these cells was influenced by how the tissue was digested, raising concerns as to its real nature. Since both ILC2 and ILC3 express ICOS, we then investigated the requirement for ICOS:ICOSL interactions in the homeostasis of ILC populations at these sites. Surprisingly, no significant differences were detected in the number of ILC1, ILC2 or ILC3 between WT and ICOSL -/- mice in any tissue, indicating that this pathway is not required for ILC homeostasis at these sites. These data were compared with CD80 -/-CD86 -/- mice given evidence of CD28 expression by some ILC and ILC crosstalk with activated T cells. Notably, the absence of CD28 ligands resulted in a significant increase in ILC2 and ILC3 numbers in the intestine. Conclusions: Together, these data provide new insight into ILC composition in different tissues in both WT and genetically modified mice where key costimulatory pathways are genetically deleted, providing a useful resource for further research into ILC biology.

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Section: Discussionmentioning

confidence: 99%

Characterisation of innate lymphoid cell populations at different sites in mice with defective T cell immunity

Dutton¹,

Camelo²,

Sleeman³

et al. 2018

Wellcome Open Res

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“…ILCs develop from common lymphoid progenitor cells whose morphology resembles that of adaptive lymphocytes. Recently, ILCs are being recognized as critical modulators of tissue homeostasis and inflammation via cytokine release [46]. ILCs can be divided into three groups based on the expression of transcriptional factors and cytokines [47]: group 1 ILCs, which include natural killer (NK) cells and ILC1s; group 2 ILCs, which consist of ILC2; and group 3 ILCs, which consist of lymphoid tissue inducer cells and NKp46and NKp46 + ILC3s [48].…”

Section: Innate Lymphoid Cells (Ilcs)mentioning

confidence: 99%

Immunophenotypic Profiles in Polycystic Ovary Syndrome

Pang

et al. 2020

Mediators of Inflammation

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Polycystic ovary syndrome (PCOS) a long-known endocrinopathy and one of the most common endocrine-reproductivemetabolic disorders in women, which can lead to infertility. Although the precise etiology remains unclear, PCOS is considered as a complex genetic trait, with a high degree of heterogeneity. Besides, hormones and immune cells, including both innate and adaptive immune cells, are reportedly a cross talk in PCOS. Chronic low-grade inflammation increases autoimmune disease risk. This proinflammatory condition may, in turn, affect vital physiological processes that ultimately cause infertility, such as ovulation failure and embryo implantation. Here, we review the accumulating evidence linking PCOS with inflammatory status providing an overview of the underlying hormone-mediated dysregulation of immune cells. We mainly focus on the correlational evidence of associations between immune status in women and the increased prevalence of PCOS, along with the specific changes in immune responses. Further recognition and exploration of these interactions may help elucidate PCOS pathophysiology and highlight targets for its treatment and prevention.

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“…Natural killer cells are one of the first responders following infection and play a role in the activation and/or maturation of dendritic cells, macrophages and T cells by producing IFN-c and TNF-a and/or killing immature dendritic cells; 41,42 they are able to kill regulatory T cells, indirectly promoting CD4 + and CD8 + effector T-cell responses, 41 and to express co-stimulatory molecules which allow them to directly promote T-cell proliferation. 43 NK cells also have a prominent pro-inflammatory role during infections owing to their ability to produce IFN-cfrequently acting as the main source of this cytokine during infection by several different bacterial pathogens, TNF-a, GM-CSF and chemokines such as nacrophage inflammatory protein-1a.…”

Section: Discussionmentioning

confidence: 99%

Natural killer cells are pivotal for in vivo protection following systemic infection by Sporothrix schenckii

et al. 2018

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Natural killer (NK) cells are one of the first cell types to enter inflammation sites and have been historically known as key effector cells against tumours and viruses; now, accumulating evidence shows that NK cells are also capable of direct in vitro activity and play a protective role against clinically important fungi in vivo. However, our understanding of NK cell development, maturation and activation in the setting of fungal infections is preliminary at best. Sporotrichosis is an emerging worldwide-distributed subcutaneous mycosis endemic in many countries, affecting humans and other animals and caused by various related thermodimorphic Sporothrix species, whose prototypical member is Sporothrix schenckii. We show that following systemic infection of BALB/c mice with S. schenckii sensu stricto, NK cells displayed a more mature phenotype as early as 5 days post-infection as judged by CD11b/CD27 expression. At 10 days post-infection, NK cells had increased expression of CD62 ligand (CD62L) and killer cell lectin-like receptor subfamily G member 1 (KLRG1), but not of CD25 or CD69. Depletion of NK cells with anti-asialo GM1 drastically impaired fungal clearance, leading to a more than eightfold increase in splenic fungal load accompanied by heightened systemic inflammation, as shown by augmented production of the pro-inflammatory cytokines tumour necrosis factor-α, interferon-γ and interleukin-6, but not interleukin-17A, in the spleen and serum. Our study is, to the best of our knowledge, the first to demonstrate that a fungal infection can drive NK cell maturation in vivo and that such cells are pivotal for in vivo protection against S. schenckii.

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Innate lymphoid cell regulation of adaptive immunity

Cited by 53 publications

References 88 publications

Characterisation of innate lymphoid cell populations at different sites in mice with defective T cell immunity

Characterisation of innate lymphoid cell populations at different sites in mice with defective T cell immunity

Immunophenotypic Profiles in Polycystic Ovary Syndrome

Natural killer cells are pivotal for in vivo protection following systemic infection by Sporothrix schenckii

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