ArticleJournal of leukocyte biology2010
TLR-mediated B cell activation results in ectopic CLIP expression that promotes B cell-dependent inflammation.
Article in Journal of leukocyte biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Sex differences in neurobehavior and the adult hippocampal neurogenic niche: influence of traumatic brain injury and CLIP antagonism.Frontiers in behavioral neuroscience · 2026Article
- Autophagy Differentially Influences Toll-like Receptor 9 and B Cell-Receptor-Mediated B Cell Expansion, Expression of Major Histocompatibility Class II Proteins, and Antigenic Peptide Presentation.International journal of molecular sciences · 2025Article
- Traumatic brain injury alters the effects of class II invariant peptide (CLIP) antagonism on chronic meningeal CLIP + B cells, neuropathology, and neurobehavioral impairment in 5xFAD mice.Journal of neuroinflammation · 2024Article
- Harnessing Innate Immunity to TreatCells · 2023Article
- TLR7 modulating B-cell immune responses in the spleen of C57BL/6 mice infected with Schistosoma japonicum.PLoS neglected tropical diseases · 2021Article
- Antagonism of Macrophage Migration Inhibitory Factory (MIF) after Traumatic Brain Injury Ameliorates Astrocytosis and Peripheral Lymphocyte Activation and Expansion.International journal of molecular sciences · 2020Article
- Antagonism of major histocompatibility complex class II invariant chain peptide during chronic lipopolysaccharide treatment rescues autoregulatory behavior.American journal of physiology. Renal physiology · 2019Article
- Vitamin D3 Suppresses Class II Invariant Chain Peptide Expression on Activated B-Lymphocytes: A Plausible Mechanism for Downregulation of Acute Inflammatory Conditions.Journal of nutrition and metabolism · 2016Article
- γδ T Cells and dendritic cells in refractory Lyme arthritis.Journal of leukocyte biology · 2015Review
- Traumatic brain injury causes selective, CD74-dependent peripheral lymphocyte activation that exacerbates neurodegeneration.Acta neuropathologica communications · 2014Article
- Immune aspects of sepsis and hope for new therapeutics.Current infectious disease reports · 2012Article
- The psychoimmunology of lyme/tick-borne diseases and its association with neuropsychiatric symptoms.The open neurology journal · 2012Article
- Lyme disease and pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS): an overview.International journal of general medicine · 2012Article
Corrections and comments
- Erratum issuedErrata.2010
- Erratum issued
Authors and funding
16 authors at 5 institutions in 2 countries.
Funding
Abstract
Infectious pathogens produce compounds called Toll ligands that activate TLRs on lymphocytes. Acute activation triggered by certain TLRs appears to "jump start" the innate immune response, characterized by the release of inflammatory cytokines and cellular expansion. In some individuals, there is a failure to control acute inflammation, resulting in postinfectious, chronic inflammation. Susceptibility to chronic inflammation is strongly associated with an individual's MHC genes. Recent clinical trials for several autoimmune diseases characterized by chronic inflammation suggest that B lymphocyte depletion therapies dampen chronic immune activation. However, currently, there is no known mechanism that accounts for the correlation among TLR activation, MHC genetics, and a pathological role for B-lymphocytes. Our hypothesis is that TLR-activated B cells (B cells that have been polyclonally activated in the absence of antigen-specific signals) are not controlled properly by T cell-dependent B cell death, thereby causing B cell-dependent chronic inflammation. Here, we show that treatment with Toll ligands results in polyclonal B cell activation accompanied by ectopic expression of CLIP. Furthermore, by adoptively transferring purified CLIP+ B cells in syngeneic animals, we find that CLIP+ B cells induce production of TNF-α by host T cells. Finally, we demonstrate that CLIP-targeted peptide competition results in the death of polyclonally activated CLIP+ B cells.
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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.