IL-22BP dictates characteristics of Peyer’s patch follicle-associated epithelium for antigen uptake

Jinnohara, Toshi; Kanaya, Takashi; Hase, Koji; Sakakibara, Sayuri; Kato, Tamotsu; Tachibana, Naoko; Sasaki, Takaharu; Hashimoto, Yusuke; Sato, Toshiro; Watarai, Hiroshi; Kunisawa, Jun; Shibata, Nao; Williams, Ifor R.; Kiyono, Hiroshi; Ohno, Hiroshi

doi:10.1084/jem.20160770

Cited by 53 publications

(53 citation statements)

References 42 publications

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“…Our data demonstrate that in the small intestine Il22ra2 transcript anatomically correlated with SILT, genetically depended on the presence of SILT, and was expressed much more highly in Yet40 + macrophages than in other macrophages, dendritic cells, or T cells. A recent report confirms some of these findings(49). This additional layer of IL-22 regulation appeared in concert with induction of IL-22 activity, as it appeared after weaning.…”

Section: Discussionsupporting

confidence: 65%

The Development of Steady-State Activation Hubs between Adult LTi ILC3s and Primed Macrophages in Small Intestine

Savage

Liang

Locksley

2017

The Journal of Immunology

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Group 3 innate lymphoid cells (ILC3s) are important for intestinal health, particularly in controlling inflammation in response to epithelial dysregulation, but their role during homeostasis remains less well understood. We generated IL-22 reporter mice to assess production of this key cytokine by ILC3s in the small intestine during development and under basal conditions. Although IL-22 is produced by a variety of lymphocyte populations, constitutively high IL-22 expression was limited to lymphoid-tissue inducer (LTi) cells residing in lymph node-like structures in the gut called small intestinal lymphoid tissues (SILT). Constitutive IL-22 expression was dependent on the microbiota and MyD88 signaling, appeared upon weaning, and was present across the spectrum of SILT, including in cryptopatches. Activated SILT LTi cells colocalized with a rare subpopulation of activated macrophages constitutively positive for IL-12/23 p40 and capable of activating neonatal LTi cells in response to TLR stimulus. Thus, weaning leads to the organization of innate immune activation hubs at SILT that mature and are continuously sustained by signals from the microbiota. This functional and anatomic organization constitutes a significant portion of the steady-state IL-23/IL-22 axis.

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Section: Discussionsupporting

confidence: 65%

The Development of Steady-State Activation Hubs between Adult LTi ILC3s and Primed Macrophages in Small Intestine

Savage

Liang

Locksley

2017

The Journal of Immunology

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“…The availability of IL‐22 is tightly regulated by IL‐22 binding protein (IL‐22BP or IL‐22Ra2), a soluble form of the IL‐22 receptor that reduces availability of IL‐22 . Genetic inactivation of IL‐22BP led to increased IL‐22 signaling in follicle‐associated epithelium and decreased access of bacteria to PP and ILF …”

Section: Ilc As Guardians Of Tissue Homeostasis Epithelial Remodelinmentioning

confidence: 99%

Innate lymphoid cells, mediators of tissue homeostasis, adaptation and disease tolerance

Branzk

Gronke

Diefenbach

2018

Immunological Reviews

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Summary Innate lymphoid cells (ILC) are a recently identified group of tissue‐resident innate lymphocytes. Available data support the view that ILC or their progenitors are deposited and retained in tissues early during ontogeny. Thereby, ILC become an integral cellular component of tissues and organs. Here, we will review the intriguing relationships between ILC and basic developmental and homeostatic processes within tissues. Studying ILC has already led to the appreciation of the integral roles of immune cells in tissue homeostasis, morphogenesis, metabolism, regeneration, and growth. This area of immunology has not yet been studied in‐depth but is likely to reveal important networks contributing to disease tolerance and may be harnessed for future therapeutic approaches.

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“…This finding is in agreement with the fact that IL22RA2 is expressed in intestinal and lymphoid tissues and that IL-22 tightly influences susceptibility to Crohn's disease and ulcerative colitis in humans. [28][29][30] Although the combination of a CNV plus an SNV accounts for a minority of autosomal recessive diseases, it could be speculated that this condition is currently underestimated due to limitations of CNV detection by whole-exome sequencing caused both by the lack of efficient pipelines able to identify such anomalies and by the possible presence of noncoding CNVs altering the expression of the disease-associated gene, consequence of both position effect and TADs (topologically associated domains) disruption mechanisms. In our case, we describe the identification of a monoallelic variant in IFNGR1, a gene whose mutations perfectly match the patient's clinical condition; thus, we hypothesize that a genomic alteration from a balanced translocation to a CNV had altered the expression of the second allele.…”

Section: Discussionmentioning

confidence: 99%

Disseminated Mycobacterium Avium Infection in a Child with Complete Interferon-γ Receptor 1 Deficiency due to Compound Heterozygosis of IFNGR1 for a Subpolymorphic Copy Number Variation and a Novel Splice-Site Variant

et al. 2019

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Complete interferon-γ receptor 1 deficiency is a monogenic primary immunodeficiency caused by IFNGR1 germline defects, with autosomal dominant or recessive inheritance, which results in invasive mycobacterial diseases with varying degrees of severity. Most of the autosomal recessive IFNGR1 mutations are homozygous loss-of-function single-nucleotide variants, whereas large genomic deletions and compound heterozygosity have been very rarely reported. Herein we describe the clinical presentation, diagnosis, and successful treatment with hematopoietic stem cell transplantation of a child with disseminated Mycobacterium avium infection due to compound heterozygosity for a subpolymorphic copy number variation and a novel splice-site variant.

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IL-22BP dictates characteristics of Peyer’s patch follicle-associated epithelium for antigen uptake

Abstract: IL-22 binding protein inhibits IL-22 signaling, which is important for intestinal homeostasis. Jinnohara et al. report that IL-22 binding protein is strongly expressed by Peyer’s patch dendritic cells and facilitates the M cell uptake of bacterial antigens into Peyer’s patches.

Cited by 53 publications

References 42 publications

The Development of Steady-State Activation Hubs between Adult LTi ILC3s and Primed Macrophages in Small Intestine

The Development of Steady-State Activation Hubs between Adult LTi ILC3s and Primed Macrophages in Small Intestine

Innate lymphoid cells, mediators of tissue homeostasis, adaptation and disease tolerance

Disseminated Mycobacterium Avium Infection in a Child with Complete Interferon-γ Receptor 1 Deficiency due to Compound Heterozygosis of IFNGR1 for a Subpolymorphic Copy Number Variation and a Novel Splice-Site Variant

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