Sympathetic innervation of murine thymus and spleen: Evidence for a functional link between the nervous and immune systems

Williams, John M.; Peterson, Richard G.; Shea, Philip A.; Schmedtje, John F.; Bauer, Dierk; Felten, David L.

doi:10.1016/s0361-9230(81)80072-x

Cited by 304 publications

(65 citation statements)

References 37 publications

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“…6-OHDA reportedly destroys noradrenergic nerve termini in the peripheral nervous system (52). In the present study, a single injection of 6-OHDA significantly decreased the NE contents of the plasma and spleens (Fig.…”

Section: Discussionsupporting

confidence: 64%

Effect of 6-Hydroxydopamine on Host Resistance againstListeria monocytogenesInfection

et al. 2001

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Recent studies have shown that immunocompetent cells bear receptors of neuropeptides and neurotransmitters and that these ligands play roles in the immune response. In this study, the role of the sympathetic nervous system in host resistance against Listeria monocytogenes infection was investigated in mice pretreated with 6-hydroxydopamine (6-OHDA), which destroys sympathetic nerve termini. The norepinephrine contents of the plasma and spleens were significantly lower in 6-OHDA-treated mice than in vehicle-treated mice. The 50% lethal dose of L. monocytogenes was about 20 times higher for 6-OHDA-treated mice than for vehicletreated mice. Chemical sympathectomy by 6-OHDA upregulated interleukin-12 (IL-12) and tumor necrosis factor-alpha (TNF-␣) production in enriched dendritic cell cultures and gamma interferon (IFN-␥) and TNF-␣ production in spleen cell cultures, whereas chemical sympathectomy had no apparent effect on phagocytic activities, listericidal activities, and nitric oxide production in peritoneal exudate cells and splenic macrophages. Augmentation of host resistance against L. monocytogenes infection by 6-OHDA was abrogated in IFN-␥ ؊/؊ or TNF-␣ ؊/؊ mice, suggesting that upregulation of IFN-␥, IL-12, and TNF-␣ production may be involved in 6-OHDA-mediated augmentation of antilisterial resistance. Furthermore, adoptive transfer of spleen cells immune to L. monocytogenes from 6-OHDA-treated mice resulted in untreated naive recipients that had a high level of resistance against L. monocytogenes infection. These results suggest that the sympathetic nervous system may modulate host resistance against L. monocytogenes infection through regulation of production of IFN-␥, IL-12, and TNF-␣, which are critical in antilisterial resistance.

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Section: Discussionsupporting

confidence: 64%

Effect of 6-Hydroxydopamine on Host Resistance againstListeria monocytogenesInfection

et al. 2001

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“…However, thymic epithelial cells have been shown to express cholinergic receptors (11,12), but the significance of these receptors remains unknown. In contrast, there are a plethora of data to show that the neurotransmitter norepinephrine that is released from sympathetic nerve endings residing within the parenchyma of lymphoid organs (13)(14)(15) in response to Ag (16), LPS (17), or IL-1␤ (18). Nerve endings containing norepinephrine directly appose lymphoid cells that express the ␤ 2 -adrenergic receptor (␤ 2 AR) which binds norepinephrine to induce an increase in the intracellular concentration of cAMP (reviewed in Refs.…”

mentioning

confidence: 99%

Stimulation of the B Cell Receptor, CD86 (B7-2), and the β2-Adrenergic Receptor Intrinsically Modulates the Level of IgG1 and IgE Produced per B Cell

Kasprowicz

Kohm

Berton

et al. 2000

The Journal of Immunology

136

129

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Our findings using B cells from either wild-type, CD86-deficient, or β2-adrenergic receptor (β2AR)-deficient mice suggest three mechanisms by which the level of IgG1 and IgE production can be increased on a per cell basis. Trinitrophenyl-specific B cells enriched from unimmunized mouse spleens were pre-exposed to Ag and/or the β2AR ligand terbutaline for 24 h before being activated by either a β2AR-negative Th2 cell clone or CD40 ligand/Sf9 cells and IL-4 in the presence or absence of an anti-CD86 Ab. Data suggest that the first mechanism involves a B cell receptor (BCR)-dependent up-regulation of CD86 expression that, when CD86 is stimulated, increases the amount of IgG1 and IgE produced in comparison to unstimulated cells. The second mechanism involves a BCR- and β2AR-dependent up-regulation of CD86 to a level higher than that induced by stimulation of either receptor alone that, when CD86 is stimulated, further increases the amount of IgG1 and IgE produced. The third mechanism is BCR-independent and involves a β2AR-dependent increase in the ability of a B cell to respond to IL-4. Flow cytometric and limiting dilution analyses suggest that the increase in IgG1 and IgE occurs independently from the isotype switching event. These findings suggest that the BCR, the β2AR, and CD86 are involved in regulating IL-4-dependent IgG1 and IgE production.

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“…Studies conducted at the University of Rochester beginning in the mid 1970's by Robert Ader (Editor-in-Chief of BBI from 1987 and Nicholas Cohen, PhD (Associate Editor during the same period) (Ader et al, 1975), likely gave rise to behavioral conditioning of T cell responses as the number one theme in the hearts of at least 2/3 of the editors! The second major theme, reflecting the research interests of David Felten, MD, PhD (Williams et al, 1980;Williams et al, 1981) (Associate Editor during the same period), involved examining the relationship between the sympathetic nervous system and primary and secondary lymphoid organs. The first of these papers to be published in BBI was from Nance et al (Nance et al, 1987); these investigators described the patterns of sympathetic innervation of the thymus.…”

Section: : Bbi's T Cell Themes Emergementioning

confidence: 99%

Brain behavior and immunity: Twenty years of T cells

Moynihan

2007

Brain, Behavior, and Immunity

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During the period from 1987-2007, our understanding of nervous system-T lymphocyte bidirectional communication advanced exponentially. Progress in exploring these relationships was aided by the constant development of new, cutting-edge technologies, and by a steady growth in interest, and number, of scientists who recognized the need to conduct cross-disciplinary research. In this brief review of 20 years of Brain, Behavior, and Immunity (BBI), we highlight just a small number of the important studies published in the journal that collectively have provided the foundation for our current understanding of brain, behavior, and, specifically, T cells.

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Sympathetic innervation of murine thymus and spleen: Evidence for a functional link between the nervous and immune systems

Cited by 304 publications

References 37 publications

Effect of 6-Hydroxydopamine on Host Resistance againstListeria monocytogenesInfection

Effect of 6-Hydroxydopamine on Host Resistance againstListeria monocytogenesInfection

Stimulation of the B Cell Receptor, CD86 (B7-2), and the β2-Adrenergic Receptor Intrinsically Modulates the Level of IgG1 and IgE Produced per B Cell

Brain behavior and immunity: Twenty years of T cells

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