Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Host-microbiota interaction is regulated by skin autonomous production of antibodies

ABSTRACT: The microbiota colonizes each barrier site and broadly controls host physiology. However, when uncontrolled, microbial colonists can also promote inflammation and induce systemic infection. The unique strategies employed at each barrier tissue to control the coexistence of the host with its microbiota remain largely elusive. Here we uncover that, within the skin, host-microbiota symbiosis depends on the remarkable ability of the skin to act as an autonomous lymphoid organ. Notably, an encounter with a new skin commensal promotes two parallel responses, both under the control of Langerhans cells. On one hand, skin commensals induce the formation of classical germinal centers within secondary lymphoid organs associated with IgG1 and IgG3 antibody responses. On the other hand, microbial colonization also leads to the development of tertiary lymphoid organs within the skin itself that can locally sustain and mature IgG2b and IgG2c responses. These phenomena are supported, at least in part, by the ability of the skin regulatory T cells to convert into T follicular helper cells that accumulate within organized tertiary lymphoid organs within the dermis. Skin autonomous production of antibodies is sufficient to control local commensal colonization as well as subsequent systemic infection with the same microbe. Collectively, these results reveal a striking compartmentalization of humoral responses to the microbiota. Further, this work uncovers a previously unappreciated function for the skin as a compartment able to develop, in the absence of inflammation, powerful and long-lived antibody responses independently of secondary lymphoid organs.

ORGANISM(S): Mus musculus

PROVIDER: GSE250572 | GEO | 2024/10/23

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Host-microbiota interaction is regulated by autonomous skin-intrinsic germinal centers [BCR]

Project description:Host symbiosis with its microbiota can represent a liability for the host. Indeed, while these communities of microbes broadly control host physiology, the microbiota can also promote inflammation and represent a source of local and systemic infection. The unique strategies employed by each tissue to maintain and control coexistence with commensal microbes remain largely unclear. Here we uncover that, within the skin, host protection from its microbiota depends on the remarkable ability of the skin to act as an autonomous lymphoid organ. Notably, an encounter with a new skin microbe is associated with two parallel responses both, under the control of Langerhans cells. On one hand, skin commensal promotes the development of classical germinal centers within secondary lymphoid organs leading to IgG1 and IgG3 responses. On the other hand, microbial colonization also leads to the development of tertiary lymphoid organs that can locally sustain and mature IgG2b and IgG2c responses. The ability of the skin to develop as a lymphoid compartment is at least in part mediated by the ability of the local Treg pool to convert into T follicular helper cells accumulating within organized tertiary lymphoid organs surrounding the hair follicles. Remarkably, skin autonomous production of antibodies is sufficient to control both microbial colonization within the skin as well as subsequent infection with the same commensal. Collectively these results reveal a profound compartmentalization of humoral responses between the lymph nodes and the skin. Further, this work uncovers a previously unappreciated function for the skin as a compartment able to develop, in the absence of inflammation, powerful and long-lived antibody responses independently of secondary lymphoid organs.

2024-10-23 | GSE279095 | GEO

Host-microbiota interaction is regulated by autonomous skin-intrinsic germinal centers

2024-10-23 | GSE272390 | GEO

Keratinocyte-intrinisic MHCII expression controls Microbiota-specific Th1 cell responses

Project description:The crosstalk between the microbiota and the immune system plays a fundamental role in the control of host physiology. However, the tissue-specific factors controlling this dialogue remain poorly understood. Here we demonstrate that T cell responses to commensal colonization are associated with the development of organized clusters within the skin epithelium. These organized lymphocyte clusters are surrounded by specialized keratinocytes expressing a discrete program associated with antigen presentation and anti-microbial defense. Notably, IL-22-mediated keratinocyte-intrinsic MHC class II expression was required for the selective accumulation of commensal-induced IFN- but not IL-17A-producing CD4+ T cells within the skin. Together, this work uncovers an unexpected role for keratinocyte-mediated antigen presentation in the licensing of homeostatic type 1 responses to the microbiota, findings that have important implications in our understanding of the unique rules governing the dialogue between the host and its microbiota.

2020-04-14 | GSE125657 | GEO

Endogenous retrovirus control of homeostatic and inflammatory responses to the microbiota [RNA-seq]

Project description:The microbiota plays a fundamental role in regulating host immunity. However, the processes that initiate homeostatic immunity to the microbiota remain largely unknown. Here, we show that the skin microbiota promotes the discrete expression of defined endogenous retrovirus (ERVs). Keratinocyte-intrinsic responses to ERVs depended on cGAS/STING signaling and promoted the induction commensal specific T cells including CD8+, CD4+ and MAIT cells. Inhibition of reverse transcriptase significantly impacted these responses resulting in impaired homeostatic immunity to the microbiota and associated tissue repair function. Conversely, diets that caused an increase in dietary lipids primed the skin for aberrant ERV expression in response to commensal colonization, leading to tissue inflammation. Together, our results support the idea that the host may have coopted its endogenous virome as a means to communicate with the exogenous microbial microbiota, resulting in a multikingdom dialogue that controls both tissue homeostasis and inflammation.

2021-05-12 | GSE158519 | GEO

Endogenous retrovirus control of homeostatic and inflammatory responses to the microbiota [RNA-seq 2]

2021-05-12 | GSE171751 | GEO

Lymphoid function of the tuberculous granuloma

Project description:Induced lymphoid structures associated with pulmonary granulomas have been observed during TB in both humans and mice and could orchestrate host defense. In order to determine whether granulomas perform lymphoid functions, mice lacking secondary lymphoid organs (SLOs) were infected with Mycobacterium tuberculosis (MTB). As in wild type mice (WT), granulomas developed, MTB was controlled, and antigen-specific T cell responses including T central memory (TCM) cells were generated in the complete absence of SLOs. Moreover, T cell activation correlated with granuloma formation in these mice and TCM cells accumulated in lungs and participated in protection against secondary MTB infection. Lung granulomas may therefore represent tertiary lymphoid organs (TLOs) capable of priming robust T cell responses and mediating host defense during chronic MTB at the site of infection.

2010-12-22 | GSE15335 | GEO

The neuroimmune CGRP-RAMP1 axis tunes cutaneous adaptive immunity to the microbiota.

Project description:The somatosensory nervous system surveils external stimuli at barrier tissues, regulating innate immune cells under infection and inflammation. The roles of sensory neurons in controlling the adaptive immune system, and more specifically immunity to the microbiota, however, remain elusive. Here, we identified a novel mechanism for direct neuroimmune communication between commensal-specific T lymphocytes and somatosensory neurons mediated by the neuropeptide calcitonin gene-related peptide (CGRP) in the skin. Intravital imaging revealed that commensal-specific T cells are in close proximity to cutaneous nerve fibers in vivo. Correspondingly, we observed upregulation of the receptor for the neuropeptide CGRP, RAMP1, in CD8+ T lymphocytes induced by skin commensal colonization. Neuroimmune CGRP-RAMP1 signaling axis functions in commensal-specific T cells to constrain Type 17 responses and moderate the activation status of microbiota-reactive lymphocytes at homeostasis. As such, modulation of neuroimmune CGRP-RAMP1 signaling in commensal-specific T cells shapes the overall activation status of the skin epithelium, thereby impacting the outcome of responses to insults such as wounding. The ability of somatosensory neurons to control adaptive immunity to the microbiota via the CGRP-RAMP1 axis underscores the various layers of regulation and multisystem coordination required for optimal microbiota-reactive T cell functions under steady state and pathology.

2024-02-21 | GSE253041 | GEO

The neuroimmune CGRP-RAMP1 axis tunes cutaneous adaptive immunity to the microbiota

2024-02-21 | GSE253063 | GEO

Rapidly induced fucosylation of intestinal epithelium sustains host-commensal symbiosis during sickness.

Project description:Systemic infection induces conserved physiological responses that include both resistance and ‘tolerance of infection’ mechanisms. Among these responses, temporary anorexia associated with an infection is often beneficial. It poses, however, a problem for the trillions of microbes residing in the gastrointestinal tract, as they also experience reduced substrate availability. We hypothesized that under anorectic conditions caused by infection, the host might activate protective mechanisms to support the gut microbiota during the acute phase of the disease. Here, we report that systemic exposure to Toll-like receptor (TLR) ligands causes rapid α1,2-fucosylation of the small intestine epithelial cells (IEC). The process requires sensing of TLR agonists and production of IL-23 by dendritic cells, activation of innate lymphoid cells and expression of α1,2-Fucosyltransferase-2 (Fut2) by IL-22-stimulated IECs. Fucosylated proteins are shed into the lumen and fucose is utilized by microbiota, as shown using reporter bacteria and by transcriptional profiling of the gut microbiome. Fucosylation also reduces the expression of bacterial virulence genes within the commensal gut microbiome and improves host tolerance of the mild pathogen Citrobacter rodentium. Thus, rapid IEC fucosylation appears to be a protective mechanism that utilizes the host’s resources to maintain host-microbial interactions during pathogen-induced stress. RNA-Seq analysis of the murine gut microbiome following LPS exposure. Fut2-/- (B6.129X1-Fut2tm1Sdo/J) mice were backcrossed greater than 7 generations to BALB/c. Fut2-/- (KO) and Fut2+/- (Het) animals were analyzed.

2014-10-24 | E-GEOD-60874 | biostudies-arrayexpress

Immunity to commensal skin fungi promotes psoriasiform skin inflammation

Project description:Under steady state conditions, the immune system is poised to sense and respond to the microbiota. As such, immunity to the microbiota, including T cell responses, is expected to precede any inflammatory trigger. How this pool of preformed microbiota-specific T cells contributes to tissue pathologies remains unclear. Here, using an experimental model of psoriasis, we show that recall responses to commensal skin fungi can significantly aggravate tissue inflammation. Enhanced pathology caused by fungi pre-exposure depends on Th17 responses and neutrophil extracellular traps and recapitulates features of the transcriptional landscape of human lesional psoriatic skin. Together, our results propose that recall responses directed to skin fungi can directly promote skin inflammation and that exploration of tissue inflammation should be assessed in the context of recall responses to the microbiota.

2020-09-22 | GSE144850 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data