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Restoration of lymphoid organ integrity through the interaction of lymphoid tissue-inducer cells with stroma of the T cell zone.

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TLDR
Crosstalk between lymphoid tissue–inducer cells and stromal cells is reactivated in adults to maintain secondary lymphoid organ integrity and thereby contributes to the preservation of immunocompetence.
Abstract
The generation of lymphoid microenvironments in early life depends on the interaction of lymphoid tissue-inducer cells with stromal lymphoid tissue-organizer cells. Whether this cellular interface stays operational in adult secondary lymphoid organs has remained elusive. We show here that during acute infection with lymphocytic choriomeningitis virus, antiviral cytotoxic T cells destroyed infected T cell zone stromal cells, which led to profound disruption of secondary lymphoid organ integrity. Furthermore, the ability of the host to respond to secondary antigens was lost. Restoration of the lymphoid microanatomy was dependent on the proliferative accumulation of lymphoid tissue-inducer cells in secondary lymphoid organs during the acute phase of infection and lymphotoxin alpha(1)beta(2) signaling. Thus, crosstalk between lymphoid tissue-inducer cells and stromal cells is reactivated in adults to maintain secondary lymphoid organ integrity and thereby contributes to the preservation of immunocompetence.

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The biology of innate lymphoid cells

TL;DR: This work summarizes the studies that formally identified innate lymphoid cells and highlights their emerging roles in controlling tissue homeostasis in the context of infection, chronic inflammation, metabolic disease and cancer.
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Human IL-25- and IL-33-responsive type 2 innate lymphoid cells are defined by expression of CRTH2 and CD161.

TL;DR: This work describes another lineage-negative CD127+CD161+ ILC population found in humans that expressed the chemoattractant receptor CRTH2 and identifies a unique type of human ILC that provides an innate source of T helper type 2 (TH2) cytokines.
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Border patrol: regulation of immunity, inflammation and tissue homeostasis at barrier surfaces by IL-22

TL;DR: How the expression of IL-22 and IL-23R is regulated, the functions of the IL- 22–IL-22R pathway in regulating immunity, inflammation and tissue homeostasis, and the therapeutic potential of targeting this pathway in human disease are discussed.
Journal ArticleDOI

Human type 1 innate lymphoid cells accumulate in inflamed mucosal tissues

TL;DR: The frequency of the ILC1 subset was much higher in inflamed intestine of people with Crohn's disease, which indicated a role for these IFN-γ-producing I LC1 cells in the pathogenesis of gut mucosal inflammation.
References
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Journal ArticleDOI

CCR7 coordinates the primary immune response by establishing functional microenvironments in secondary lymphoid organs.

TL;DR: In this paper, the chemokine receptor CCR7 was identified as an important organizer of the primary immune response in mice, and severely delayed kinetics regarding the antibody response and lack contact sensitivity and delayed type hypersensitivity reactions.
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Structure and function of the spleen.

TL;DR: The spleen enables it to remove older erythrocytes from the circulation and leads to the efficient removal of blood-borne microorganisms and cellular debris, which makes it the most important organ for antibacterial and antifungal immune reactivity.
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Fas and Perforin Pathways as Major Mechanisms of T Cell-Mediated Cytotoxicity

TL;DR: The perforin- and Fas-based mechanisms may account for all T cell-mediated cytotoxicity in short-term in vitro assays, and no third mechanism was detected.
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A chemokine-driven positive feedback loop organizes lymphoid follicles

TL;DR: It is established that B-lymphocyte chemoattractant (BLC/BCA1) and its receptor, CXCR5, are needed for B-cell homing to follicles in lymph nodes as well as in spleen, and that BLC is required for the development of most lymph nodes and Peyer's patches.
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Mice Lacking Expression of Secondary Lymphoid Organ Chemokine Have Defects in Lymphocyte Homing and Dendritic Cell Localization

TL;DR: It is suggested that the abnormalities in plt mice are due to a genetic defect in the expression of SLC and that SLC mediates the entry of naive T cells and antigen-stimulated DCs into the T cell zones of secondary lymphoid organs.
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