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

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

PROVIDER: PRJNA1054551 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27292729_1.fastq.gz	Fastqsanger.gz
	SRR27292729_2.fastq.gz	Fastqsanger.gz
	SRR27292730_1.fastq.gz	Fastqsanger.gz
	SRR27292730_2.fastq.gz	Fastqsanger.gz
	SRR27292731_1.fastq.gz	Fastqsanger.gz

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

Project description: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.

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

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

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

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.

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

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