ArticleThe Journal of experimental medicine2002
B cell-dependent T cell responses: IgM antibodies are required to elicit contact sensitivity.
Article in The Journal of experimental medicine, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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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
37 citing papers in PubMed, 118 citations in OpenAlex.
- Hapten-Specific Cellular Immune Responses in the Elicitation and Sensitization Phases of Murine Contact Hypersensitivity.Biomolecules · 2025Article
- Extracellular Vesicle (EV) Targeted Cells Release Secondary Effector EVs: Indication of How To Account for Histocompatibility and Disease Specificity of EV Treatments.Journal of extracellular vesicles · 2025Review
- Impact of IDO1 and IDO2 on the B Cell Immune Response.Frontiers in immunology · 2022Review
- Article
- COVID-19 therapy with mesenchymal stromal cells (MSC) and convalescent plasma must consider exosome involvement: Do the exosomes in convalescent plasma antagonize the weak immune antibodies?Journal of extracellular vesicles · 2020Review
- Orally Administered Exosomes Suppress Mouse Delayed-Type Hypersensitivity by Delivering miRNA-150 to Antigen-Primed Macrophage APC Targeted by Exosome-Surface Anti-Peptide Antibody Light Chains.International journal of molecular sciences · 2020Article
- The Dynamics of the Skin's Immune System.International journal of molecular sciences · 2019Review
- Antibody Light Chains Dictate the Specificity of Contact Hypersensitivity Effector Cell Suppression Mediated by Exosomes.International journal of molecular sciences · 2018Article
- Natural Killer Cell Memory: Progress and Implications.Frontiers in immunology · 2017Review
- Metal nanoparticles in the presence of lipopolysaccharides trigger the onset of metal allergy in mice.Nature nanotechnology · 2016Article
- IDO2 Modulates T Cell-Dependent Autoimmune Responses through a B Cell-Intrinsic Mechanism.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- A subset of AID-dependent B-1a cells initiates hypersensitivity and pneumococcal pneumonia resistance.Annals of the New York Academy of Sciences · 2015Review
- From Mysterious Supernatant Entity to miRNA-150 in Antigen-Specific Exosomes: a History of Hapten-Specific T Suppressor Factor.Archivum immunologiae et therapiae experimentalis · 2015Review
- Hapten-induced contact hypersensitivity, autoimmune reactions, and tumor regression: plausibility of mediating antitumor immunity.Journal of immunology research · 2014Review
- Disruption of the complement anaphylatoxin receptor C5L2 exacerbates inflammation in allergic contact dermatitis.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Natural killer cell-mediated contact sensitivity develops rapidly and depends on interferon-α, interferon-γ and interleukin-12.Immunology · 2013Article
- Impaired humoral immunity and tolerance in K14-VEGFR-3-Ig mice that lack dermal lymphatic drainage.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Early immune events in the induction of allergic contact dermatitis.Nature reviews. Immunology · 2012Review
- Regulatory B cells and allergic diseases.Allergy, asthma & immunology research · 2011Article
- Contributions of antinucleoprotein IgG to heterosubtypic immunity against influenza virus.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
Abstract
Contact sensitivity (CS) is a classic example of in vivo T cell immunity in which skin sensitization with reactive hapten leads to immunized T cells, which are then recruited locally to mediate antigen-specific inflammation after subsequent skin challenge. We have previously shown that T cell recruitment in CS is triggered by local activation of complement, which generates C5a that triggers C5a receptors most likely on mast cells. Here, we show that B-1 cell-derived antihapten IgM antibodies generated within 1 day (d) of immunization combine with local challenge antigen to activate complement to recruit the T cells. These findings overturn three widely accepted immune response paradigms by showing that (a) specific IgM antibodies are required to initiate CS, which is a classical model of T cell immunity thought exclusively due to T cells, (b) CS priming induces production of specific IgM antibodies within 1 d, although primary antibody responses typically begin by day 4, and (c) B-1 cells produce the 1-d IgM response to CS priming, although these cells generally are thought to be nonresponsive to antigenic stimulation. Coupled with previous evidence, our findings indicate that the elicitation of CS is initiated by rapidly formed IgM antibodies. The IgM and challenge antigen likely form local complexes that activate complement, generating C5a, leading to local vascular activation to recruit the antigen-primed effector T cells that mediate the CS 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.