ArticleCellular immunology2010
Murine mammary carcinoma cells and CD11c(+) dendritic cells elicit distinct responses to lipopolysaccharide and exhibit differential expression of genes required for TLR4 signaling.
Article in Cellular immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Quercetin inhibits the activity and function of dendritic cells through the TLR4/IRAK4/NF-κB signalling pathway.Contemporary oncology (Poznan, Poland) · 2023Article
- Controlling cancer-induced inflammation with a nucleic acid scavenger prevents lung metastasis in murine models of breast cancer.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- The Central THαβ Immunity Associated Cytokine: IL-10 Has a Strong Anti-Tumor Ability Toward Established Cancer ModelsFrontiers in oncology · 2021Article
- Article
- A Multifaceted Role for Myd88-Dependent Signaling in Progression of Murine Mammary Carcinoma.Breast cancer : basic and clinical research · 2016Article
- A role for HMGB1, HSP60 and Myd88 in growth of murine mammary carcinoma in vitro.Cellular immunology · 2013Article
- Growth, metastasis, and expression of CCL2 and CCL5 by murine mammary carcinomas are dependent upon Myd88.Cellular immunology · 2012Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Although TLR are often studied on DC because of their ability to bridge innate and adaptive defenses, TLR are also expressed by epithelial cells. Because the majority of cancers are carcinomas, and thus of epithelial origin, we wanted to know whether a carcinoma and DC responded similarly to a TLR agonist. We found the mammary carcinoma 4T1 and CD11c(+) DC both secreted proinflammatory chemokines in response to the TLR4 agonist lipopolysaccharide (LPS). However a clear dichotomy existed. DC, but not 4T1 secreted IL-1β, TNF-α, and upregulated CD80 and CD86 expression following LPS treatment. A potential reason for differential responsiveness was that DC expressed greater levels of TLR4, CD14, Myd88, and TRAM. Despite the low level of TLR signaling proteins, the carcinoma were able to elicit a range of responses contingent upon the source, dose, length, and frequency of TLR agonist treatment. Thus, carcinoma and DC are distinctly responsive to LPS.
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Registered trials
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