ArticleInfection and immunity2006
Role for the CD28 molecule in the control of Coxiella burnetii infection.
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 10 papers.
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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
10 citing papers in PubMed, 26 citations in OpenAlex.
- T-Bet Controls Susceptibility of Mice toFrontiers in microbiology · 2020Article
- Early Cytokine Response After Vaccination withJournal of veterinary research · 2018Article
- A fatal case of disseminated chronic Q fever: a case report and brief review of the literature.Infection · 2016Review
- In the absence of its cytosolic domain, the CD28 molecule still contributes to T cell activation.Cellular and molecular life sciences : CMLS · 2015Article
- CD28 deletion improves obesity-induced liver steatosis but increases adiposity in mice.International journal of obesity (2005) · 2015Article
- Early cytokine and antibody responses against Coxiella burnetii in aerosol infection of BALB/c mice.Diagnostic microbiology and infectious disease · 2015Article
- CD28 homodimer interface mimetic peptide acts as a preventive and therapeutic agent in models of severe bacterial sepsis and gram-negative bacterial peritonitis.The Journal of infectious diseases · 2015Article
- Article
- An experimental mouse model to establish Tropheryma whipplei as a diarrheal agent.The Journal of infectious diseases · 2011Article
- Persistent Coxiella burnetii infection in mice overexpressing IL-10: an efficient model for chronic Q fever pathogenesis.PLoS pathogens · 2008Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Q fever is an infectious disease caused by Coxiella burnetii, an obligate intracellular bacterium that replicates in macrophages. As cell-mediated immune response to microbial pathogens requires signals mediated by T-cell receptors and costimulatory molecules such as CD28, we wondered if CD28 is involved in protection against C. burnetii infection. CD28-deficient (CD28-/-) mice were inoculated with C. burnetii by intraperitoneal and intravenous routes. With both wild-type and CD28-/- mice, C. burnetii organisms were detected exclusively in spleen and liver. The antibody response against C. burnetii was impaired in CD28-/- animals, but, surprisingly, the lack of CD28 decreased C. burnetii burden in the infected tissues, whatever the manner of inoculation of bacteria. The CD28 deficiency had no effect on either granuloma formation, which reflects cell-mediated immunity against C. burnetii, or the production of gamma interferon and tumor necrosis factor, two cytokines known to be involved in granuloma formation. On the other hand, the production of interleukin-10 (IL-10) by peritoneal macrophages was highly impaired in CD28-/- mice. The results suggest that CD28 initiates a signal that favors C. burnetii replication through the modulation of the IL-10 pathway.
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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.