Abstract
The role of vitamin A in the various parts of the immune system remains elusive. Toll-like receptors (TLRs) are involved in innate polyclonal activation of B-cells, and as such they are important for maintaining long-lasting first line defense against pathogens. Here we explore the impact of all-trans retinoic acid (RA) on B cell responses mediated via the TLR homolog RP105 (CD180). We show that RA slightly reduces the proliferation and IgG production in CD27+ memory B cells stimulated by anti-RP105 alone. However, co-stimulation with the TLR9-ligand CpG results in turning RA into a potent stimulator of RP105-induced proliferation and IgG synthesis in memory B cells. The results emphasize the important role of RA in stimulating TLR-mediated polyclonal activation and differentiation of B cells, and reveal the complex interplay between various TLRs that may underlie the ability of RA to fight pathogens.
Copyright © 2012 Elsevier Inc. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antibodies / pharmacology
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Antigens, CD / immunology
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Antigens, CD / metabolism*
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B-Lymphocytes / drug effects*
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B-Lymphocytes / immunology
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B-Lymphocytes / metabolism
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Cell Proliferation / drug effects*
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Cells, Cultured
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Dose-Response Relationship, Drug
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Drug Synergism
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Enzyme-Linked Immunosorbent Assay
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Flow Cytometry
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Humans
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Immunoglobulin G / biosynthesis*
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Immunologic Memory / immunology
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Interleukin-10 / immunology
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Interleukin-10 / metabolism
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Oligodeoxyribonucleotides / pharmacology
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Signal Transduction / drug effects
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Toll-Like Receptor 9 / agonists
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Toll-Like Receptor 9 / metabolism*
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Tretinoin / pharmacology*
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Tumor Necrosis Factor Receptor Superfamily, Member 7 / immunology
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Tumor Necrosis Factor Receptor Superfamily, Member 7 / metabolism
Substances
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Antibodies
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Antigens, CD
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CD180 protein, human
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Immunoglobulin G
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Oligodeoxyribonucleotides
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TLR9 protein, human
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Toll-Like Receptor 9
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Tumor Necrosis Factor Receptor Superfamily, Member 7
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Interleukin-10
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Tretinoin