ArticleInfection and immunity2006
Interleukin-10 anti-inflammatory response to Borrelia burgdorferi, the agent of Lyme disease: a possible role for suppressors of cytokine signaling 1 and 3.
Article in Infection and immunity, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
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Who cites it
25 citing papers in PubMed, 60 citations in OpenAlex.
- Innate Immune Evasion of Lyme Disease Pathogen Drives Alzheimer-Like Pathology.Research square · 2026Article
- Strain-specific immune response patterns toInfection and immunity · 2026Article
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- A chemosensory-like histidine kinase is dispensable for chemotaxis in vitro but regulates the virulence of Borrelia burgdorferi through modulating the stability of RpoS.PLoS pathogens · 2023Article
- Immune Response toCurrent issues in molecular biology · 2021Article
- Suppressors of Cytokine Signaling (SOCS)1 and SOCS3 Proteins Are Mediators of Interleukin-10 Modulation of Inflammatory Responses Induced byMediators of inflammation · 2020Article
- Prolonged Release and Functionality of Interleukin-10 Encapsulated within PLA-PEG Nanoparticles.Nanomaterials (Basel, Switzerland) · 2019Article
- SOCS Proteins as Regulators of Inflammatory Responses Induced by Bacterial Infections: A Review.Frontiers in microbiology · 2017Review
- Lyme borreliosis.Nature reviews. Disease primers · 2016Review
- SOCS3 revisited: a broad regulator of disease, now ready for therapeutic use?Cellular and molecular life sciences : CMLS · 2016Review
- SOCS1/3 expression levels in HSV-1-infected, cytokine-polarized and -unpolarized macrophages.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2015Article
- MicroRNA-146a provides feedback regulation of lyme arthritis but not carditis during infection with Borrelia burgdorferi.PLoS pathogens · 2014Article
- Phagosomal TLR signaling upon Borrelia burgdorferi infection.Frontiers in cellular and infection microbiology · 2014Review
- 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
- Article
- Interleukin-10 alters effector functions of multiple genes induced by Borrelia burgdorferi in macrophages to regulate Lyme disease inflammation.Infection and immunity · 2011Article
- The role of the immuno-inflammatory response in patients after cardiac arrest.Archives of medical science : AMS · 2011Article
- Impairment of gamma interferon signaling in human neutrophils infected with Anaplasma phagocytophilum.Infection and immunity · 2010Article
- CD14 signaling restrains chronic inflammation through induction of p38-MAPK/SOCS-dependent tolerance.PLoS pathogens · 2009Article
- SOCS1 and SOCS3 in the control of CNS immunity.Trends in immunology · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
It has been established that interleukin-10 (IL-10) inhibits inflammatory cytokines produced by macrophages in response to Borrelia burgdorferi or its lipoproteins. The mechanism by which IL-10 exerts this anti-inflammatory effect is still unknown. Recent findings indicate that suppressors of cytokine signaling (SOCS) proteins are induced by cytokines and Toll-like receptor (TLR)-mediated stimuli, and in turn they can down-regulate cytokine and TLR signaling in macrophages. Because it is known that SOCS are induced by IL-10 and that B. burgdorferi and its lipoproteins most likely interact via TLR2 or the heterodimers TLR2/1 and/or TLR2/6, we hypothesized that SOCS are induced by IL-10 and B. burgdorferi and its lipoproteins in macrophages and that SOCS may mediate the inhibition by IL-10 of concomitantly elicited cytokines. We report here that mouse J774 macrophages incubated with IL-10 and added B. burgdorferi spirochetes (freeze-thawed, live, or sonicated) or lipidated outer surface protein A (L-OspA) augmented their SOCS1/SOCS3 mRNA and protein expression, with SOCS3 being more abundant. Pam(3)Cys, a synthetic lipopeptide, also induced SOCS1/SOCS3 expression under these conditions, but unlipidated OspA was ineffective. Neither endogenous IL-10 nor the translation inhibitor cycloheximide blocked SOCS1/SOCS3 induction by B. burgdorferi and its lipoproteins, indicating that the expression of other genes is not required. This temporally correlated with the IL-10-mediated inhibition of the inflammatory cytokines IL-1beta, IL-6, IL-12p40, IL-18, and tumor necrosis factor alpha. Our data are evidence to suggest that expression of SOCS is part of the mechanism of IL-10-mediated inhibition of inflammatory cytokines elicited by B. burgdorferi and its lipoproteins.
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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.