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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<jats:italic>B. burgdorferi<\/jats:italic>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<jats:italic>B. burgdorferi<\/jats:italic>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<jats:italic>B. burgdorferi<\/jats:italic>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<jats:sub>3<\/jats:sub>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<jats:italic>B. burgdorferi<\/jats:italic>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-1\u03b2, IL-6, IL-12p40, IL-18, and tumor necrosis factor \u03b1. 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<jats:italic>B. burgdorferi<\/jats:italic>and its lipoproteins.<\/jats:p>","DOI":"10.1128\/iai.00678-06","type":"journal-article","created":{"date-parts":[[2006,9,20]],"date-time":"2006-09-20T23:06:35Z","timestamp":1158793595000},"page":"5780-5789","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":41,"title":["Interleukin-10 Anti-Inflammatory Response to<i>Borrelia burgdorferi<\/i>, the Agent of Lyme Disease: a Possible Role for Suppressors of Cytokine Signaling 1 and 3"],"prefix":"10.1128","volume":"74","author":[{"given":"Vida A.","family":"Dennis","sequence":"first","affiliation":[{"name":"Division of Bacteriology and Parasitology, Tulane National Primate Research Center, Tulane University Health Sciences Center, Covington, Louisiana"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ayanna","family":"Jefferson","sequence":"additional","affiliation":[{"name":"Division of Bacteriology and Parasitology, Tulane National Primate Research Center, Tulane University Health Sciences Center, Covington, Louisiana"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shree R.","family":"Singh","sequence":"additional","affiliation":[{"name":"Department of Math and Science, Alabama State University, Montgomery, Alabama"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fre\u0301de\u0301ric","family":"Ganapamo","sequence":"additional","affiliation":[{"name":"Division of Immunology, Tulane National Primate Research Center, Tulane University Health Sciences Center, Covington, Louisiana"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mario T.","family":"Philipp","sequence":"additional","affiliation":[{"name":"Division of Bacteriology and Parasitology, Tulane National Primate Research Center, Tulane University Health Sciences Center, Covington, Louisiana"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/nri818"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.immunol.22.091003.090312"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M410992200"},{"key":"e_1_3_2_5_2","first-page":"263","volume":"139","year":"1991","unstructured":"Barthold, S. 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