ReviewMedical microbiology and immunology2010
CD28 and IL-4: two heavyweights controlling the balance between immunity and inflammation.
Review in Medical microbiology and immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
14 citing papers in PubMed, 24 citations in OpenAlex.
- CD28-signaling can be partially compensated in CD28-knockout mice but is essential for virus elimination in a murine model of multiple sclerosis.Frontiers in immunology · 2023Article
- How sphingolipids affect T cells in the resolution of inflammation.Frontiers in pharmacology · 2022Review
- A high frequency of CD8International journal of medical sciences · 2018Article
- CD28 days later: Resurrecting costimulation for CD8(+) memory T cells.European journal of immunology · 2016Article
- Article
- Inducible deletion of CD28 prior to secondary nippostrongylus brasiliensis infection impairs worm expulsion and recall of protective memory CD4⁺ T cell responses.PLoS pathogens · 2014Article
- Expression pattern of serum cytokines in hepatitis B virus infected patients with persistently normal alanine aminotransferase levels.Journal of clinical immunology · 2013Article
- Reversing T cell immunosenescence: why, who, and how.Age (Dordrecht, Netherlands) · 2013Review
- Molecular immunologic correlates of spontaneous latency in a rabbit model of pulmonary tuberculosis.Cell communication and signaling : CCS · 2013Article
- IL1B, IL4R, IL12RB1 and TNF gene polymorphisms are associated with Plasmodium vivax malaria in Brazil.Malaria journal · 2012Article
- Recent publications in medical microbiology and immunology: a retrospective.Medical microbiology and immunology · 2012Review
- Comparison of pro-inflammatory cytokine expression and cellular signal transduction in human macrophages infected with different influenza A viruses.Medical microbiology and immunology · 2011Article
- Role of dendritic cell maturity/costimulation for generation, homeostasis, and suppressive activity of regulatory T cells.Frontiers in immunology · 2011Article
- Host adaptive immunity deficiency in severe pandemic influenza.Critical care (London, England) · 2010Article
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 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The costimulatory receptor CD28 and IL-4Ralpha containing cytokine receptors play key roles in controlling the size and quality of pathogen-specific immune responses. Thus, CD28-mediated costimulation is needed for effective primary T-cell expansion and for the generation and activation of regulatory T-cells (Treg cells), which protect from immunopathology. Similarly, IL-4Ralpha signals are required for alternative activation of macrophages, which counteract inflammation by type 1 responses. Furthermore,immune modulation by CD28 and IL-4 is interconnected through the promotion of IL-4 producing T-helper 2 cells by CD28 signals. Using conditionally IL-4Ralpha and CD28 deleting mice, as well as monoclonal antibodies, which block or stimulate CD28, or mAb that deplete Treg cells, we have studied the roles of CD28 and IL-4Ralpha in experimental mouse models of virus (influenza), intracellular bacteria (L. monocytogenes, M. tuberculosis), and parasite infections (T. congolense, L. major). We observed that in some, but not all settings, Treg cells and type 2 immune deviation, including activation of alternative macrophages can be manipulated to protect the host either from infection or from immunopathology with an overall beneficial outcome. Furthermore, we provide direct evidence that secondary CD8 T-cell responses to i.c. bacteria are dependent on CD28-mediated costimulation.
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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.