ArticleJournal of immunology (Baltimore, Md. : 1950)2009
CD21/35 promotes protective immunity to Streptococcus pneumoniae through a complement-independent but CD19-dependent pathway that regulates PD-1 expression.
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 23 papers.
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Who cites it
23 citing papers in PubMed, 29 citations in OpenAlex.
- Activation of B1 B cells by F. tularensis atypical LPS depends on classical complement and C3a.PLoS pathogens · 2025Article
- The role of B-1 cells in cancer progression and anti-tumor immunity.Frontiers in immunology · 2024Review
- Role of regulation of PD-1 and PD-L1 expression in sepsis.Frontiers in immunology · 2023Review
- The Antidepressant Mirtazapine Rapidly Shifts Hepatic B Cell Populations and Functional Cytokine Signatures in the Mouse.Frontiers in immunology · 2021Article
- B Cell Subsets Differentially Contribute to the T Cell-Independent Memory Pool.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- The regulators of BCR signaling during B cell activation.Blood science (Baltimore, Md.) · 2019Review
- Highly homogenous tri-acylated S-LPS acts as a novel clinically applicable vaccine against Shigella flexneri 2a infection.Vaccine · 2019Article
- PD-1 immunobiology in systemic lupus erythematosus.Journal of autoimmunity · 2019Review
- CD22 Promotes B-1b Cell Responses to T Cell-Independent Type 2 Antigens.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- B-1 lymphocytes in mice and nonhuman primates.Annals of the New York Academy of Sciences · 2015Review
- PD-1 suppresses protective immunity to Streptococcus pneumoniae through a B cell-intrinsic mechanism.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- C4 Deficiency is a predisposing factor for Streptococcus pneumoniae-induced autoantibody production.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Alterations in the peripheral blood B cell subpopulations of multidrug-resistant tuberculosis patients.Clinical and experimental medicine · 2014Article
- Aging promotes B-1b cell responses to native, but not protein-conjugated, pneumococcal polysaccharides: implications for vaccine protection in older adults.The Journal of infectious diseases · 2014Article
- Generation of a novel Cr2 gene allele by homologous recombination that abrogates production of Cr2 but is sufficient for expression of Cr1.Immunobiology · 2014Article
- Optimal germinal center B cell activation and T-dependent antibody responses require expression of the mouse complement receptor Cr1.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- PD-1 Interaction with PD-L1 but not PD-L2 on B-cells Mediates Protective Effects of Estrogen against EAE.Journal of clinical & cellular immunology · 2013Article
- Primate B-1 cells generate antigen-specific B cell responses to T cell-independent type 2 antigens.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Marginal zone B cells: virtues of innate-like antibody-producing lymphocytes.Nature reviews. Immunology · 2013Review
- Programmed cell death 1 suppresses B-1b cell expansion and long-lived IgG production in response to T cell-independent type 2 antigens.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Humoral immunity to T cell-independent type 2 Ags (TI-2 Ag) is critical for protection against encapsulated bacteria such as Streptococcus pneumoniae. The CD21/35 receptor is thought to promote protective humoral immunity to encapsulated bacteria by enabling complement-decorated capsular polysaccharides to coligate the CD21/35-CD19 signaling complex with the B cell Ag receptor (BCR), thereby enhancing Ag-specific B cell activation. However, Ab responses to S. pneumoniae type 3 capsular polysaccharide (PPS-3) and other strong TI-2 Ags were significantly impaired in CD21/35(-/-) but not C3(-/-) or C4(-/-) mice. B cells from CD21/35(-/-) mice expressed significantly higher levels of cell surface CD19. CD21/35(-/-) B cells exhibited enhanced BCR-induced calcium responses and significantly higher expression of the inhibitory programmed death-1 (PD-1) receptor following immunization with a TI-2 Ag or BCR crosslinking. Reducing CD19 expression in CD21/35(-/-) mice normalized BCR-induced calcium responses, PD-1 induction, and PPS-3-specific IgG3 responses and restored protection during S. pneumoniae infection. PD-1 blockade also selectively rescued PPS-3-specific IgG3 responses in CD21/35(-/-) mice. Thereby, CD21/35 promotes protective humoral immunity to S. pneumoniae and other strong TI-2 Ags through a complement-independent pathway by negatively regulating CD19 expression and PD-1 induction.
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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.