ArticleJournal of immunotoxicology
Asbestos activates CH12.LX B-lymphocytes via macrophage signaling.
Article in Journal of immunotoxicology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- B-1 cells in immunotoxicology: Mechanisms underlying their response to chemicals and particles.Frontiers in toxicology · 2023Review
- Late Inflammation Induced by Asbestiform Fibers in Mice Is Ameliorated by a Small Molecule Synthetic Lignan.International journal of molecular sciences · 2021Article
- Exploring Animal Models That Resemble Idiopathic Pulmonary Fibrosis.Frontiers in medicine · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
The impact of asbestos exposure on the development and progression of autoimmunity is becoming increasingly recognized as a public health issue. Epidemiological studies have shown an association between exposure to airborne silicates, such as asbestos, and autoimmunity, but the etiology remains unresolved. B1a B-lymphocytes have been implicated in autoimmune responses in mice, and splenic B1a cell numbers are altered following asbestos exposure. The purpose of this study was to explore the possible role of B1a B-lymphocytes in the production of pathogenic autoantibodies by testing the hypothesis that B1a B-lymphocytes directly react with asbestos and increase production of antibodies. The B1a-like B-lymphocyte model, CH12.LX, was exposed to asbestos in vitro via direct and indirect mechanisms. The effect was determined of these exposures on the rate of proliferation and on production of various immunoglobulin classes. Direct exposure elicited no measurable response by the CH12.LX cells. Culturing the CH12.LX cells in media from asbestos-exposed RAW 264.7 macrophages, however, decreased the proliferation rate and stimulated the cells to increase production of the immunoglobulin isotypes IgG₁, IgG₃, and IgA. It was discovered that asbestos stimulated the macrophages to increase production of the cytokines interleukin (IL)-6 and tumor necrosis factor (TNF)-α. Recombinant murine IL-6 caused similar results seen with the macrophage media, indicating a role of IL-6 in stimulating a response by the B1a B-lymphocytes to asbestos. In correlation with the in vitro data, it was determined ex vivo that exposure of peritoneal cells (from C57Bl/6 mice) to asbestos caused an increase in the expression of IL-6 and TNFα, as well as of surface expression of IgA on the peritoneal B1a B-lymphocytes. These data demonstrate that asbestos leads to immunologic changes consistent with activation of B1a B-lymphocytes. This study also provides a model for analyzing the critical steps that may be involved in asbestos-induced autoimmune responses.
Indexed as
Identifiers
What OpenQuestion holds
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.