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Open AccessJournal ArticleDOI

TLR agonists regulate alloresponses and uncover a critical role for donor APCs in allogeneic bone marrow rejection.

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TLDR
It is shown that CpG ODNs markedly accelerated graft-versus-host disease (GVHD) lethality by Toll-like receptor 9 (TLR9) ligation of host antigen-presenting cells (APCs), dependent upon host IFNgamma but independent of host IL-12, IL-6, or natural killer cells.
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This article is published in Blood.The article was published on 2008-10-15 and is currently open access. It has received 77 citations till now. The article focuses on the topics: TLR9 & Antigen-presenting cell.

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Journal ArticleDOI

Multipotent mesenchymal stromal cells and the innate immune system

TL;DR: It is important to study the crosstalk between MSCs and innate immunity, which ranges from the bone marrow niche to injured tissue, and to identify components of the innate immune system also have a key role.
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MyD88/TLR9 mediated immunopathology and gut microbiota dynamics in a novel murine model of intestinal graft-versus-host disease

TL;DR: The important role of TLR9-mediated immunopathology was independently confirmed by significantly reduced macroscopic disease symptoms and colonic apoptosis as well as by reduced T-cell and neutrophil numbers within the colon after treatment with a synthetic inhibitory oligonucleotide.
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New perspectives on the biology of acute GVHD

TL;DR: A novel perspective on the immunobiology of acute GVHD is provided and some of the outstanding questions and limitations of the model systems are discussed.
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Graft-versus-host disease: regulation by microbe-associated molecules and innate immune receptors

TL;DR: These insights identify important mechanisms regarding the induction of GVHD through the interplay of microbial molecules and innate immunity, thus opening a new area for future therapeutic approaches.
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Inducing the tryptophan catabolic pathway, indoleamine 2,3-dioxygenase (IDO), for suppression of graft-versus-host disease (GVHD) lethality

TL;DR: It is shown that upon arrival in the colon, activated donor T cells produced interferon-gamma that up-regulated IDO, causing T-cell anergy and apoptosis, and it is concluded that IDO up-regulation may have therapeutic potential for preventing GVHD in the clinic.
References
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Journal ArticleDOI

Innate Immune Recognition

TL;DR: Microbial recognition by Toll-like receptors helps to direct adaptive immune responses to antigens derived from microbial pathogens to distinguish infectious nonself from noninfectious self.
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Cpg motifs in bacterial dna trigger direct b-cell activation

TL;DR: The potent immune activation by CpG oligon nucleotides has impli-cations for the design and interpretation of studies using 'antisense' oligonucleotides and points to possible new applications as adjuvants.
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Toll-like receptors in innate immunity.

TL;DR: Toll-like receptors-mediated activation of innate immunity controls not only host defense against pathogens but also immune disorders, and the involvement of TLR-mediated pathways in autoimmune and inflammatory diseases has been proposed.
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Small anti-viral compounds activate immune cells via the TLR7 MyD88-dependent signaling pathway.

TL;DR: It is shown that the imidazoquinolines activate immune cells via the Toll-like receptor 7 (TLR7)-MyD88–dependent signaling pathway, and that neither MyD88- nor TLR7-deficient mice showed any inflammatory cytokine production by macrophages, proliferation of splenocytes or maturation of dendritic cells.
Journal ArticleDOI

CpG Motifs in Bacterial DNA and Their Immune Effects

TL;DR: Oligodeoxynucleotides containing CpG ODN enhance the development of acquired immune responses for prophylactic and therapeutic vaccination and protect against lethal challenge with a wide variety of pathogens.
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