ArticleJournal of leukocyte biology2008
An antibody against the surfactant protein A (SP-A)-binding domain of the SP-A receptor inhibits T cell-mediated immune responses to Mycobacterium tuberculosis.
Article in Journal of leukocyte biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
- Endogenous hepcidin plays an essential role inEmerging microbes & infections · 2025Article
- Role of pattern recognition receptors in sensingHeliyon · 2023Review
- Genomic and epigenomic adaptation in SP-R210 (Myo18A) isoform-deficient macrophages.Immunobiology · 2021Article
- Structural and Functional Determinants of Rodent and Human Surfactant Protein A: A Synthesis of Binding and Computational Data.Frontiers in immunology · 2019Article
- Elevated Cyclic AMP Inhibits Mycobacterium tuberculosis-Stimulated T-cell IFN-γ Secretion Through Type I Protein Kinase A.The Journal of infectious diseases · 2018Article
- Local amplifiers of IL-4Rα-mediated macrophage activation promote repair in lung and liver.Science (New York, N.Y.) · 2017Article
- Identification of CD245 as myosin 18A, a receptor for surfactant A: A novel pathway for activating human NK lymphocytes.Oncoimmunology · 2016Article
- SP-R210 (Myo18A) Isoforms as Intrinsic Modulators of Macrophage Priming and Activation.PloS one · 2015Article
- Early secreted antigenic target of 6-kDa protein of Mycobacterium tuberculosis primes dendritic cells to stimulate Th17 and inhibit Th1 immune responses.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Surfactant protein A integrates activation signal strength to differentially modulate T cell proliferation.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Prolonged survival of scavenger receptor class A-deficient mice from pulmonary Mycobacterium tuberculosis infection.Tuberculosis (Edinburgh, Scotland) · 2011Article
- The Mycobacterium tuberculosis early secreted antigenic target of 6 kDa inhibits T cell interferon-γ production through the p38 mitogen-activated protein kinase pathway.The Journal of biological chemistry · 2011Article
- Surfactant protein A (SP-A)-mediated clearance of Staphylococcus aureus involves binding of SP-A to the staphylococcal adhesin eap and the macrophage receptors SP-A receptor 210 and scavenger receptor class A.The Journal of biological chemistry · 2011Article
- Characterization of Virulence Factors of Staphylococcus aureus: Novel Function of Known Virulence Factors That Are Implicated in Activation of Airway Epithelial Proinflammatory Response.Journal of pathogens · 2011Article
- Mycobacterium Tuberculosis Infection and Inflammation: what is Beneficial for the Host and for the Bacterium?Frontiers in microbiology · 2011Article
- P63 (CKAP4) as an SP-A receptor: implications for surfactant turnover.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2010Review
- Pulmonary surfactant: an immunological perspective.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2010Review
- ESAT-6 inhibits production of IFN-gamma by Mycobacterium tuberculosis-responsive human T cells.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- SP-R210 isoforms of Myosin18A modulate endosomal sorting and recognition of influenza A virus infection in macrophages.Microbes and infectionArticle
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Surfactant protein A (SP-A) suppresses lymphocyte proliferation and IL-2 secretion, in part, by binding to its receptor, SP-R210. However, the mechanisms underlying this effect are not well understood. Here, we studied the effect of antibodies against the SP-A-binding (neck) domain (alpha-SP-R210n) or nonbinding C-terminal domain (alpha-SP-R210ct) of SP-R210 on human peripheral blood T cell immune responses against Mycobacterium tuberculosis. We demonstrated that both antibodies bind to more than 90% of monocytes and 5-10% of CD3+ T cells in freshly isolated PBMC. Stimulation of PBMC from healthy tuberculin reactors [purified protein derivative-positive (PPD+)] with heat-killed M. tuberculosis induced increased antibody binding to CD3+ cells. Increased antibody binding suggested enhanced expression of SP-R210, and this was confirmed by Western blotting. The antibodies (alpha-SP-R210n) cross-linking the SP-R210 through the SP-A-binding domain markedly inhibited cell proliferation and IFN-gamma secretion by PBMC from PPD+ donors in response to heat-killed M. tuberculosis, whereas preimmune IgG and antibodies (alpha-SP-R210ct) cross-linking SP-R210 through the non-SP-A-binding, C-terminal domain had no effect. Anti-SP-R210n also decreased M. tuberculosis-induced production of TNF-alpha but increased production of IL-10. Inhibition of IFN-gamma production by alpha-SP-R210n was abrogated by the combination of neutralizing antibodies to IL-10 and TGF-beta1. Together, these findings support the hypothesis that SP-A, via SP-R210, suppresses cell-mediated immunity against M. tuberculosis via a mechanism that up-regulates secretion of IL-10 and TGF-beta1.
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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.