Copycat innate lymphoid cells dampen gut inflammation

Magri, Giuliana; Cerutti, Andrea

doi:10.1038/cr.2015.79

Cited by 3 publications

(8 citation statements)

References 12 publications

(26 reference statements)

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“…A failure of ILC2 development could play a role, as a recent study described that peripheral blood CD117 + ILCs include unipotent and multipotent ILC precursors, and reduction of these ILC precursors might be involved in the deficiency of CD117 + ILCs in CVID [33]. As a possible further explanation, an intrinsic NFKB signaling defect as described previously in CVID could hamper ILC2 development and/or expansion, as ILC activation and function are critically dependent upon TNFRSF members [22,[34][35][36]. The observed diminished expression of IL2R is likely to impair proliferative response to IL2-stimulation, resulting in an inability of ILC2 to expand upon activation.…”

Section: Discussionmentioning

confidence: 78%

“…A subset of CVID patients suffers from chronic enteropathy manifested as chronic non‐infectious diarrhea, malabsorption, weight loss and symptoms and findings resembling inflammatory bowel disease or gluten enteropathy . It has recently been shown that CD117 + ILC (comprising ILC3 and the majority of ILC2) maintain gut homeostasis, such as controlling inflammatory T cell responses to the intestinal bacterial flora . A defect in CD117 + ILC‐mediated regulation of proinflammatory T cells was found in the gut of patients with inflammatory bowel syndrome indicating that an impairment of ILC‐mediated immune regulation could cause gut inflammation .…”

Section: Resultsmentioning

confidence: 99%

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Reduced numbers of circulating group 2 innate lymphoid cells in patients with common variable immunodeficiency

Geier¹,

Kraupp²,

Bra³

et al. 2017

Eur J Immunol

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Recent studies identified an emerging role of group 2 and 3 innate lymphoid cells (ILCs) as key players in the generation of T-dependent and T-independent antibody production. In this retrospective case-control study, CD117 ILCs (including the majority of ILC2 and ILC3) were reduced in patients with common variable immunodeficiency (CVID). The reduction in CD117 ILCs was distinctive to CVID and could not be observed in patients with X-linked agammaglobulinemia. Patients with a more pronounced reduction in CD117 ILC numbers showed significantly lower numbers of peripheral MZ-like B cells and an increased prevalence of chronic, non-infectious enteropathy. Subsequent phenotyping of ILC subsets in CVID revealed that the reduction in CD117 ILC numbers is due to a reduction in ILC2 numbers. In vitro expansion of CVID ILC2 in response to IL-2, IL-7, IL-25 and IL-33 was impaired. Furthermore, upregulation of MHCII and IL-2RA in response to IL-2, IL-7, IL-25 and IL-33 was impaired in CVID ILC2. Thus, our results indicate a dysregulation of ILC subsets with a reduction in ILC2 numbers in CVID, however, further studies are needed to explore whether ILC abnormalities are a primary finding or secondary to disease complications encountered in CVID.

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Section: Discussionmentioning

confidence: 78%

Section: Resultsmentioning

confidence: 99%

Reduced numbers of circulating group 2 innate lymphoid cells in patients with common variable immunodeficiency

Geier¹,

Kraupp²,

Bra³

et al. 2017

Eur J Immunol

View full text Add to dashboard Cite

show abstract

“…In addition, IL-1β regulates the release of Csf2 by ILC3, which promotes the secretion of retinoic acid (RA) and IL-10 from DCs and macrophages to generate homeostasis in the gut ( 73 ). ILC3 acquires antigen from CD103 + DCs in LP and eliminates commensal-reactive CD4 + T cells in the mLN during homeostasis ( 74 ). ILC3 T cell interaction inhibits IL-2 production and induces apoptosis of effector CD4 + T cells ( 74 ).…”

Section: Molecular Mechanism Of Ccr9 + Dcs In Inflmentioning

confidence: 99%

“…ILC3 acquires antigen from CD103 + DCs in LP and eliminates commensal-reactive CD4 + T cells in the mLN during homeostasis ( 74 ). ILC3 T cell interaction inhibits IL-2 production and induces apoptosis of effector CD4 + T cells ( 74 ). However, in IBD, this function is compromised due to the low expression of MHC-II on ILC3, which governs the expansion of pathogenic Th17 cells ( 74 ).…”

Section: Molecular Mechanism Of Ccr9 + Dcs In Inflmentioning

confidence: 99%

“…ILC3 T cell interaction inhibits IL-2 production and induces apoptosis of effector CD4 + T cells ( 74 ). However, in IBD, this function is compromised due to the low expression of MHC-II on ILC3, which governs the expansion of pathogenic Th17 cells ( 74 ). Hepworth et al shows that ILC3 and thymic epithelial cells show regulation of MHC-II expression, and MHC-II + ILC3s can directly induce cell death in activated commensal bacteria-specific CD4 + T cells ( 75 ).…”

Section: Molecular Mechanism Of Ccr9 + Dcs In Inflmentioning

confidence: 99%

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The Regulatory Function of CCR9+ Dendritic Cells in Inflammation and Autoimmunity

Pathak

Lal

2020

Front. Immunol.

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Chemokine receptor CCR9 is a G protein–coupled receptor and expressed on several types of immune cells, including dendritic cells (DCs), CD4 + T cells, and B cells. CCR9 drives the migration of immune cells to gradients of its cognate ligand CCL25. The chemokine CCL25 is mostly produced by gut and thymic epithelial cells. Gut- and thymic-homing DCs are known to express CCR9, and these cells are predominantly localized in the gut lining and thymus. CCR9 + DCs are implicated in regulating inflammation, food allergy, alloimmunity, and autoimmunity. Differential interaction of CCR9 + DCs with lymphoid and myeloid cells in the thymus, secondary lymphoid tissues, and mucosal sites offer crucial insights to immune regulation. In this review, we examine the phenotypes, distributions, and interactions of CCR9 + DCs with other immune cells, elucidating their functions and role in inflammation and autoimmunity.

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Role of rare immune cells in common variable immunodeficiency

Soltani

Rezaei

Fekrvand

et al. 2022

Pediatric Allergy Immunology

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Common variable immunodeficiency disorder (CVID) is the most frequent symptomatic inborn errors of immunity (IEIs) 1 with an estimated prevalence of 1:50,000-1:25,000. 2 CVID is characterized by hypogammaglobulinemia, impaired production of specific immunoglobulin (Ig), and increased susceptibility to recurrent infections. Clinical manifestations in CVID patients demonstrate a wide spectrum of complications including recurrent infections, pulmonary complications, granulomatous or polyclonal lymphocytic infiltrations, autoimmunity, gastrointestinal diseases, and neoplasia, which can be established in different periods of life, from childhood to late adulthood. 3,4 Immunoglobulin replacement therapy is the most important therapeutic intervention for decreasing chronic infections and infectious sequels of these patients. 5

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Copycat innate lymphoid cells dampen gut inflammation

Cited by 3 publications

References 12 publications

Reduced numbers of circulating group 2 innate lymphoid cells in patients with common variable immunodeficiency

Reduced numbers of circulating group 2 innate lymphoid cells in patients with common variable immunodeficiency

The Regulatory Function of CCR9+ Dendritic Cells in Inflammation and Autoimmunity

Role of rare immune cells in common variable immunodeficiency

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