ArticleJournal of immunology (Baltimore, Md. : 1950)2016
The Costimulatory Molecule ICOS Regulates Host Th1 and Follicular Th Cell Differentiation in Response to Plasmodium chabaudi chabaudi AS Infection.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 56 citations in OpenAlex.
- The LEF1-LAG3 axis regulates CD4Parasites & vectors · 2026Article
- Cellular and molecular interactions underlying the peripheral immune responses to blood-stage malaria infections.ImmunoHorizons · 2026Review
- Inducible T-Cell Co-Stimulator (ICOS) and ICOS Ligand: Dealing With a Two-Faced Cancer Immunoregulatory System.Cancer medicine · 2026Review
- Asymptomatic vivax malaria is associated with an IFN-γ-program on adaptive immunity.Journal of translational medicine · 2025Article
- Article
- Synergistic blockade of TIGIT and PD-L1 increases type-1 inflammation and improves parasite control during murine blood-stageInfection and immunity · 2024Article
- ATG5-regulated CCL2/MCP-1 production in myeloid cells selectively modulates anti-malarial CD4Autophagy · 2024Article
- The differentiation courses of the Tfh cells: a new perspective on autoimmune disease pathogenesis and treatment.Bioscience reports · 2024Review
- Bhlhe40 limits early IL-10 production from CD4Infection and immunity · 2023Article
- Cellular iron governs the host response to malaria.PLoS pathogens · 2023Article
- Research Progress of Dendritic Cell Surface Receptors and Targeting.Biomedicines · 2023Review
- A T follicular helper cell origin for T regulatory type 1 cells.Cellular & molecular immunology · 2023Article
- T cell co-stimulatory and co-inhibitory pathways in atopic dermatitis.Frontiers in immunology · 2023Review
- Review
- ICOS Expression Is Required for Maintenance but Not the Formation of Germinal Centers in the Spleen in Response to Plasmodium yoelii Infection.Infection and immunity · 2022Article
- Inducible Costimulator-C-X-C Motif Chemokine Receptor 3 Signaling is Involved in Chronic Obstructive Pulmonary Disease Pathogenesis.International journal of chronic obstructive pulmonary disease · 2022Article
- The spleen: "epicenter" in malaria infection and immunity.Journal of leukocyte biology · 2021Review
- Cytokine-skewed Tfh cells: functional consequences for B cell help.Trends in immunology · 2021Review
- T-follicular helper cells in malaria infection and roles in antibody induction.Oxford open immunology · 2021Review
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Blood-stage Plasmodium chabaudi chabaudi AS infection requires cell- and Ab-mediated immunity to control acute and persistent infection, respectively. ICOS regulates CD4(+) T cell activation and promotes the induction of follicular Th (TFH) cells, CD4(+) T cells that support B cell affinity maturation within germinal centers (GCs), resulting in the production of high-affinity Abs. In this article, we demonstrate that, in response to P. c. chabaudi AS infection, the absence of ICOS resulted in an enhanced Th1 immune response that reduced peak parasitemia. Despite the absence of ICOS, CD4(+) T cells were capable of expressing PD-1, B cell lymphoma 6, and CXCR5 during early infection, indicating TFH development was not impaired. However, by day 21 postinfection, Icos(-/-) mice accumulated fewer splenic TFHs compared with Icos(+/+) mice, leading to substantially fewer GC B cells and a decrease in affinity, but not production, of parasite-specific isotype-switched Abs. Moreover, treatment of mice with anti-ICOS ligand Abs to modulate ICOS-ICOS ligand signaling revealed a requirement for ICOS in TFH differentiation only after day 6 postinfection. Ultimately, the quality and quantity of isotype-switched Abs produced in Icos(-/-) mice declined over time, resulting in impaired control of persistent parasitemia. Collectively, these data suggest ICOS is not required for TFH induction during P. c. chabaudi AS infection or production of isotype-switched Abs, but it is necessary for maintenance of a sustained high-affinity, protective Ab response.
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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.