ArticleJournal of immunology (Baltimore, Md. : 1950)2009
Pertussis toxin signals through the TCR to initiate cross-desensitization of the chemokine receptor CXCR4.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
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
26 citing papers in PubMed, 45 citations in OpenAlex.
- Expression of the CXCR4 S338X Variant Improves Anti-Leukemia Efficacy of Anti-CD19 CAR-T Cells.Cancer science · 2026Article
- CXCL12+ fibroblastic reticular cells in lymph nodes facilitate immune tolerance by regulating T cell-mediated alloimmunity.The Journal of clinical investigation · 2025Article
- The Neonatal Immune System and Respiratory Pathogens.Microorganisms · 2023Review
- T cell egress via lymphatic vessels is tuned by antigen encounter and limits tumor control.Nature immunology · 2023Article
- Novel murine model reveals an early role for pertussis toxin in disrupting neonatal immunity toFrontiers in immunology · 2023Article
- Pertussis toxin suppresses dendritic cell-mediated delivery of B. pertussis into lung-draining lymph nodes.PLoS pathogens · 2022Article
- Contribution of a Novel Pertussis Toxin-Like Factor in Mediating Persistent Otitis Media.Frontiers in cellular and infection microbiology · 2022Article
- Pertussis Toxin Inhibits Encephalitogenic T-Cell Infiltration and Promotes a B-Cell-Driven Disease during Th17-EAE.International journal of molecular sciences · 2021Article
- Single-Molecule, Super-Resolution, and Functional Analysis of G Protein-Coupled Receptor Behavior Within the T Cell Immunological Synapse.Frontiers in cell and developmental biology · 2020Article
- Type I Interferon Therapy Limits CNS Autoimmunity by Inhibiting CXCR3-Mediated Trafficking of Pathogenic Effector T Cells.Cell reports · 2019Article
- Mobilized peripheral blood: an updated perspective.F1000Research · 2019Review
- Role of Major Toxin Virulence Factors in Pertussis Infection and Disease Pathogenesis.Advances in experimental medicine and biology · 2019Article
- Article
- Contribution of pertussis toxin to the pathogenesis of pertussis disease.Pathogens and disease · 2015Review
- CBAP promotes thymocyte negative selection by facilitating T-cell receptor proximal signaling.Cell death & disease · 2014Article
- Toward a mechanism-based in vitro safety test for pertussis toxin.Human vaccines & immunotherapeutics · 2014Review
- Chemokines in the balance: maintenance of homeostasis and protection at CNS barriers.Frontiers in cellular neuroscience · 2014Review
- The B subunit of an AB5 toxin produced by Salmonella enterica serovar Typhi up-regulates chemokines, cytokines, and adhesion molecules in human macrophage, colonic epithelial, and brain microvascular endothelial cell lines.Infection and immunity · 2013Article
- Comparative genomics of the classical Bordetella subspecies: the evolution and exchange of virulence-associated diversity amongst closely related pathogens.BMC genomics · 2012Article
- Ectopic expression of the immune adaptor protein CD3zeta in neural stem/progenitor cells disrupts cell-fate specification.Journal of molecular neuroscience : MN · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Pertussis toxin (PTx) has been shown to exert a variety of effects on immune cells independent of its ability to ADP-ribosylate G proteins. Of these effects, the binding subunit of PTx (PTxB) has been shown to block signaling via the chemokine receptor CCR5, but the mechanism involved in this process is unknown. Here, we show that PTxB causes desensitization of a related chemokine receptor, CXCR4, and explore the mechanism by which this occurs. CXCR4 is the receptor for the chemokine stromal cell-derived factor 1alpha (SDF-1alpha) and elicits a number of biological effects, including stimulation of T cell migration. PTxB treatment causes a decrease in CXCR4 surface expression, inhibits G protein-associated signaling, and blocks SDF-1alpha-mediated chemotaxis. We show that PTxB mediates these effects by activating the TCR signaling network, as the effects are dependent on TCR and ZAP70 expression. Additionally, the activation of the TCR with anti-CD3 mAb elicits a similar set of effects on CXCR4 activity, supporting the idea that TCR signaling leads to cross-desensitization of CXCR4. The inhibition of CXCR4 by PTxB is rapid and transient; however, the catalytic activity of PTx prevents CXCR4 signaling in the long term. Thus, the effects of PTx holotoxin on CXCR4 signaling can be divided into two phases: short term by the B subunit, and long term by the catalytic subunit. These data suggest that TCR crosstalk with CXCR4 is likely a normal cellular process that leads to cross-desensitization, which is exploited by the B subunit of PTx.
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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.