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Vasoactive intestinal peptide differentially modulates human immunoglobulin production
1Department of Pediatrics, Kyoto University Hospital, Japan.
Advances in Neuroimmunology
|January 1, 1996
Summary
Vasoactive intestinal peptide (VIP) differentially modulates human immunoglobulin production. VIP enhances IgA1, IgG1, and IgM in B cell lines, while selectively inducing IgA1/IgA2 in non-atopic donors and inhibiting IgE/IgG4 in atopic patients.
Area of Science:
- Immunology
- Endocrinology
- Cell Biology
Background:
- Vasoactive intestinal peptide (VIP) is a neuropeptide with known immunomodulatory functions.
- The precise effects of VIP on human immunoglobulin (Ig) production across different B cell subsets and conditions remain incompletely understood.
- Understanding these interactions is crucial for exploring therapeutic strategies targeting immune responses.
Purpose of the Study:
- To investigate the specific effects of VIP on human immunoglobulin production in various B cell contexts.
- To determine whether VIP's influence on Ig production is mediated by other cytokines or signaling pathways.
- To elucidate the differential impact of VIP on B cells from non-atopic donors versus atopic patients.
Main Methods:
- Human B cell lines (GM-1056, IM-9, CBL) were treated with VIP, somatostatin (SOM), or substance P (SP).
- Anti-CD40 mAb-stimulated B cells from non-atopic donors and unstimulated mononuclear cells from atopic patients were analyzed.
- VIP's effects were assessed in the presence of VIP antagonists, cytokine antagonists, and various co-culture conditions (T cells, monocytes).
Main Results:
- VIP dose-dependently enhanced IgA1, IgG1, and IgM production in specific B cell lines, an effect blocked by VIP antagonists but not cytokine antagonists.
- In non-atopic donors, VIP selectively stimulated IgA1 and IgA2 production in B cells expressing surface IgA1 and IgA2, respectively.
- Conversely, in atopic patients, VIP inhibited spontaneous IgE and IgG4 production, particularly when B cells were co-cultured with both T cells and monocytes.
Conclusions:
- VIP exerts specific and context-dependent effects on human immunoglobulin production.
- VIP's modulatory actions on Ig production are independent of common cytokines like IL-6 and IL-10 and are mediated via VIP-specific receptors.
- VIP demonstrates potential as a therapeutic agent, capable of selectively enhancing beneficial IgA responses or suppressing detrimental IgE/IgG4 production in specific immune contexts.