Mobilisation of specific T cells from lymph nodes in contact sensitivity requires substance P

Shepherd, Andrew J.; Beresford, Lorna; Bell, Eric B.; Miyan, Jaleel

doi:10.1016/j.jneuroim.2005.04.008

Cited by 23 publications

(22 citation statements)

References 68 publications

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“…Functionally, this may reflect the fact that lymph nodes collect and process immune cells from specific regions of the body, all of which receive an extensive afferent sensory innervation (skin, muscle, mucosa, etc.). Sensory fibers are important regulators of localized inflammatory responses in skin and the extension of this neural-immune interaction into the draining lymph nodes appears likely (Shepherd et al, 2005). Also, unlike the thymus and spleen, lymph nodes process immune responses that are associated with specific regions of the body and tissue compartments where the location of the immune challenge would be critical for directing the immune system to sites of injury and infection.…”

Section: Innervation Of Lymph Nodesmentioning

confidence: 99%

“…The adjuvant-like contribution of sensory fibers to the local actions of microbes and antigens at these body surfaces represent a significant modulator of the magnitude and effectiveness of the localized inflammatory (innate) immune response, as well as the subsequent adaptive immune response (Shepherd et al, 2005).…”

Section: Other Sites Of Neuroimmune Regulationmentioning

confidence: 99%

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Autonomic innervation and regulation of the immune system (1987–2007)

Nance¹,

Sanders²

2007

Brain, Behavior, and Immunity

746

580

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Since 1987, only a few neuroanatomical studies have been conducted to identify the origin of innervation for the immune system. These studies demonstrated that all primary and secondary immune organs receive a substantial sympathetic innervation from sympathetic postganglionic neurons. Neither the thymus nor spleen receive any sensory neural innervation; however, there is evidence that lymph nodes and bone marrow may be innervated by sensory neurons located in dorsal root ganglia. There is no neuroanatomical evidence for a parasympathetic or vagal nerve supply to any immune organ. Thus, the primary pathway for the neural regulation of immune function is provided by the sympathetic nervous system (SNS) and its main neurotransmitter, norepinephrine (NE). Activation of the SNS primarily inhibits the activity of cells associated with the innate immune system, while it either enhances or inhibits the activity of cells associated with the acquired/adaptive immune system. Innate immune cells express both alpha and beta-adrenergic receptor subtypes, while T and B lymphocytes express adrenergic receptors of the beta2 subtype exclusively, except for murine Th2 cells that lack expression of any subtype. Via these adrenergic receptors, NE is able to regulate the level of immune cell activity by initiating a change in the level of cellular activity, which often involves a change in the level of gene expression for cytokines and antibodies.

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Section: Innervation Of Lymph Nodesmentioning

confidence: 99%

Section: Other Sites Of Neuroimmune Regulationmentioning

confidence: 99%

Autonomic innervation and regulation of the immune system (1987–2007)

Nance¹,

Sanders²

2007

Brain, Behavior, and Immunity

746

580

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“…First, as noted, exercise alters circulating factors and mediators (e.g., lactate, IL-6, catecholamines, growth hormone) that can affect t-cells [8][9][10]. Secondly, lymphocytes could be influenced by more direct effects such as exercise associated neurostimulation of lymph nodes and other lymph tissues [11,12]. Finally, some of the immune effects of exercise are mechanical.…”

Section: Introductionmentioning

confidence: 99%

Serum from exercising humans suppresses t-cell cytokine production

Radom‐Aizik¹,

Leu²,

Zaldivar³

2007

Cytokine

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Exercise affects t-cell cytokine production. Whether or not these effects are caused by circulating factors associated with physical activity (e.g., inflammatory mediators, acidosis) is unknown. To investigate this, we incubated sera (10%), obtained from 16 young-adults before (PRE) and after (END) 30-min of exercise, with commercially available Jurkat cells, a t-lymphocyte model, that, of course, had never been exposed to an exercise milieu. After 1-h and 6-h in culture, we measured in the supernatant four cytokines (each known to be altered by exercise and involved in disease pathophysiology): IL-2, TGF-β1, TNF-α, and IL-1ra. Cell proliferation was assessed with proliferating nuclear cell antigen (PNCA). Statistical analysis consisted of a linear mixed model for repeated measurement. There was no effect of exercise on t-cell production of either TGF-β1 or IL-1ra. In contrast, both IL-2 (p=0.025) and TNF-α (p=0.031) production was significantly suppressed in sera from the exercising participants. The suppression of these two cytokines occurred despite the fact that PNCA significantly increased (p<0.0001) in the END serum. In conclusion, exercise alters circulating factors that can, subsequently, influence t-cell cytokine production in vitro.

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“…As a means to understand the contribution of substance P in the sensitivity of 6OHDA-treated mice to ocular HSV-1 infection, the neurokinin 1 receptor (NK1R) antagonist, L703,606 (Shepherd et al, 2005) was administered to 6OHDA-treated mice at times after HSV-1 infection. Treatment of sympathectomized mice with the NK1R antagonist was found to delay mortality by 3 days although eventually the survival rate was similar to vehicle-treated, sympathectomized mice.…”

Section: Discussionmentioning

confidence: 99%

Chemical sympathectomy increases susceptibility to ocular herpes simplex virus type 1 infection

Templeton

Nguyen

Ash

et al. 2008

Journal of Neuroimmunology

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The cornea is one of the most highly innervated tissues in the mammalian host. We hypothesized changes to cornea innervation through chemical sympathectomy would significantly alter the host response to the neurotropic viral pathogen, herpes simplex virus type 1 (HSV-1) following ocular infection. Mice treated with 6-hydroxydopamine hydrobromide displayed reduced tyrosine hydroxylase-positive fibers residing in the cornea. Sympathectomized mice were also found to show a transient rise in virus recovered in infected tissues and succumbed to infection in greater numbers. Whereas there were no differences in infiltrating leukocyte populations including HSV-1-specific cytotoxic T lymphocytes in the infected tissue, an increase in substance P and a decrease in IFN-γ levels in the trigeminal ganglion but not brain stem of sympathectomized mice were noted. Sympathectomized mice treated with the neurokinin-1 receptor antagonist L703,606 had delayed mortality implicating the involvement of substance P in HSV-1-mediated death.

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Mobilisation of specific T cells from lymph nodes in contact sensitivity requires substance P

Cited by 23 publications

References 68 publications

Autonomic innervation and regulation of the immune system (1987–2007)

Autonomic innervation and regulation of the immune system (1987–2007)

Serum from exercising humans suppresses t-cell cytokine production

Chemical sympathectomy increases susceptibility to ocular herpes simplex virus type 1 infection

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