ArticleJournal of immunology (Baltimore, Md. : 1950)2002
Murine Lyme arthritis development mediated by p38 mitogen-activated protein kinase activity.
Article in Journal of immunology (Baltimore, Md. : 1950), 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 39 citations in OpenAlex.
- Article
- The AxBioTick study - immune gene expression signatures in human skin bitten by Borrelia-infected versus non-infected ticks.BMC infectious diseases · 2024Article
- Tick sialostatins L and L2 differentially influence dendritic cell responses to Borrelia spirochetes.Parasites & vectors · 2015Article
- The MEK/ERK pathway is the primary conduit for Borrelia burgdorferi-induced inflammation and P53-mediated apoptosis in oligodendrocytes.Apoptosis : an international journal on programmed cell death · 2014Article
- Macrophage p38 mitogen-activated protein kinase activity regulates invariant natural killer T-cell responses during Borrelia burgdorferi infection.The Journal of infectious diseases · 2012Article
- Localized production of IL-10 suppresses early inflammatory cell infiltration and subsequent development of IFN-γ-mediated Lyme arthritis.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Role of adrenomedullin in Lyme disease.Infection and immunity · 2010Article
- Downstream signals for MyD88-mediated phagocytosis of Borrelia burgdorferi can be initiated by TRIF and are dependent on PI3K.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- Neurogenic exacerbation of microglial and astrocyte responses to Neisseria meningitidis and Borrelia burgdorferi.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- c-Jun N-terminal kinase 1 is required for Toll-like receptor 1 gene expression in macrophages.Infection and immunity · 2007Article
- Role of novel protein kinase C isoforms in Lyme arthritis.Cellular microbiology · 2007Article
- Anti-p19 antibody treatment exacerbates lyme arthritis and enhances borreliacidal activity.Clinical and vaccine immunology : CVI · 2007Article
- p38 mitogen-activated protein kinase controls NF-kappaB transcriptional activation and tumor necrosis factor alpha production through RelA phosphorylation mediated by mitogen- and stress-activated protein kinase 1 in response to Borrelia burgdorferi antigens.Infection and immunity · 2007Article
- Control of Borrelia burgdorferi-specific CD4+-T-cell effector function by interleukin-12- and T-cell receptor-induced p38 mitogen-activated protein kinase activity.Infection and immunity · 2006Article
- Inhibition of interleukin-17 prevents the development of arthritis in vaccinated mice challenged with Borrelia burgdorferi.Infection and immunity · 2003Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Borrelia burgdorferi, the Lyme disease agent, causes joint inflammation in an experimental murine model. Inflammation occurs, in part, due to the ability of B. burgdorferi to induce the production of proinflammatory cytokines and a strong CD4(+) T helper type 1 response. The mechanisms by which spirochetes induce these responses are not completely known, although transcription factors, such as NF-kappa B in phagocytic cells, initiate the proinflammatory cytokine burst. We show here that the mitogen-activated protein (MAP) kinase of 38 kDa (p38 MAP kinase) is involved in the proinflammatory cytokine production elicited by B. burgdorferi Ags in phagocytic cells and the development of murine Lyme arthritis. B. burgdorferi Ags activated p38 MAP kinase in vitro, and the use of a specific inhibitor repressed the spirochete-induced production of TNF-alpha. The infection of mice that are deficient for a specific upstream activator of the kinase, MAP kinase kinase 3, resulted in diminished proinflammatory cytokine production and the development of arthritis, without compromising the ability of CD4(+) T cells to respond to borrelial Ags or the production of specific Abs. Overall, these data indicated that the p38 MAP kinase pathway plays an important role in B. burgdorferi-elicited inflammation and point to potential new therapeutic approaches to the treatment of inflammation induced by the spirochete.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.