ArticleImmunology2006
Interleukin-4-dependent innate collaboration between iNKT cells and B-1 B cells controls adaptative contact sensitivity.
Article in Immunology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 39 citations in OpenAlex.
- Wenqing Yin Attenuates the Allergic Contact Dermatitis Response by Inhibiting the JAK2/STAT1 and MAPK Signaling Pathways.Journal of inflammation research · 2025Article
- Antibody Light Chains Dictate the Specificity of Contact Hypersensitivity Effector Cell Suppression Mediated by Exosomes.International journal of molecular sciences · 2018Article
- Allergic Contact Dermatitis Evaluation: Strategies for the Preschooler.Current allergy and asthma reports · 2018Review
- A subset of AID-dependent B-1a cells initiates hypersensitivity and pneumococcal pneumonia resistance.Annals of the New York Academy of Sciences · 2015Review
- Estriol strongly inhibits DNCB-induced contact dermatitis: role of antigen-specific antibodies in pathogenesis.Endocrine connections · 2014Article
- Hapten-induced contact hypersensitivity, autoimmune reactions, and tumor regression: plausibility of mediating antitumor immunity.Journal of immunology research · 2014Review
- Coincidence of autoantibody production with the activation of natural killer T cells in α-galactosylceramide-mediated hepatic injury.Immunology · 2011Article
- Mechanism of dinitrochlorobenzene-induced dermatitis in mice: role of specific antibodies in pathogenesis.PloS one · 2009Article
- Effects of plant alkylphenols on cytokine production, tyrosine nitration and inflammatory damage in the efferent phase of contact hypersensitivity.British journal of pharmacology · 2007Article
- Macrophages and neutrophils are the targets for immune suppression by glucocorticoids in contact allergy.The Journal of clinical investigation · 2007Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
We showed that hepatic Valpha14+ invariant natural killer T (iNKT) cells, via their rapid interleukin (IL)-4 production, activate B-1 cells to initiate contact sensitivity (CS). This innate collaboration was absent in IL-4(-/-) and signal transducer and activator of transcription (STAT)-6(-/-) mice and was inhibited by anti-IL-4 treatment. These mice have defective CS because they fail to locally recruit the sensitized effector T cells of acquired immunity. Their CS is reconstituted by transfer of downstream-acting 1-day immune B-1 cells from wild-type mice. Responses were not reconstituted with B-1 cells from IL-4 receptor-alpha(-/-) or STAT-6(-/-) mice, nor by IL-4 treatment of B cell-deficient mice at immunization. Finally, IL-4 was preferentially and transiently produced by hepatic iNKT cells within 7 min after sensitization to mediate collaboration between innate-like iNKT cells and the B-1 B cells that participate in the recruitment of effector T cells in vivo.
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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.