Cytokine Production by Naive and Primary Effector CD4+ T Cells Exposed to Norepinephrine

Ramer-Quinn, D S; Swanson, Michelle A.; Lee, William T.; Sanders, Virginia M.

doi:10.1006/brbi.2000.0603

Cited by 67 publications

(54 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Stimulation of either β-or β 2 -AR inhibits mitogen-or anti-CD3 antibody-induced T cell proliferation [146,149,[191][192][193][194][195][196], and particularly inhibits naïve T cells differentiation into Th1 cells [139][140][141]197,198] by affecting early events involved in the initiation of proliferation [199]. β-AR-mediated inhibition of T cell proliferation may be explained, at least in part, by its ability to inhibit IL-2R expression and/ or IL-2 production by activated T cells [139,140,146,191,[200][201][202][203][204][205][206].…”

Section: Functional Significance Of Sympathetic Innervation Of Secondmentioning

confidence: 99%

Sympathetic modulation of immunity: Relevance to disease

Bellinger

Millar

Perez

et al. 2008

Cellular Immunology

225

185

View full text Add to dashboard Cite

Optimal host defense against pathogens requires cross-talk between the nervous and immune systems. This paper reviews sympathetic-immune interaction, one major communication pathway, and its importance for health and disease. Sympathetic innervation of primary and secondary immune organs is described, as well as evidence for neurotransmission with cells of the immune system as targets. Most research thus far as focused on neural-immune modulation in secondary lymphoid organs, and have revealed complex sympathetic modulation resulting in both potentiation and inhibition of immune functions. SNS-immune interaction may enhance immune readiness during disease-or injury-induced 'fight' responses. Research also indicate that dysregulation of the SNS can significantly affect the progression of immune-mediated diseases. However, a better understanding of neural-immune interactions is needed to develop strategies for treatment of immune-mediated diseases that are designed to return homeostasis and restore normal functioning neural-immune networks.

show abstract

Section: Functional Significance Of Sympathetic Innervation Of Secondmentioning

confidence: 99%

Sympathetic modulation of immunity: Relevance to disease

Bellinger

Millar

Perez

et al. 2008

Cellular Immunology

225

185

View full text Add to dashboard Cite

show abstract

“…Indeed, sympathetic fibers reach primary and secondary lymphoid organs including the spleen, thymus, and lymph nodes (11,12), where they terminate near or in direct contact with lymphocytes. The presence of adrenergic receptors (AR) 3 on lymphocytes suggests that sympathetic innervation may be important in the modulation of immune responses (3,13). Although neuronal influences on lymphocytes have been explored, their effect on professional APC has only begun to be studied.…”

mentioning

confidence: 99%

Catecholamines Inhibit the Antigen-Presenting Capability of Epidermal Langerhans Cells

Seiffert¹,

Hosoi²,

Torii³

et al. 2002

The Journal of Immunology

119

View full text Add to dashboard Cite

The sympathetic nervous system modulates immune function at a number of levels. Within the epidermis, APCs (Langerhans cells (LC)) are frequently anatomically associated with peripheral nerves. Furthermore, some neuropeptides have been shown to regulate LC Ag-presenting function. We explored the expression of adrenergic receptors (AR) in murine LC and assessed their functional role on Ag presentation and modulation of cutaneous immune responses. Both purified LC and the LC-like cell lines XS52-4D and XS106 expressed mRNA for the ARs α1A and β2. XS106 cells and purified LC also expressed β1-AR mRNA. Treatment of murine epidermal cell preparations with epinephrine (EPI) or norepinephrine inhibited Ag presentation in vitro. Furthermore, pretreatment of epidermal cells with EPI or norepinephrine in vitro suppressed the ability of these cells to present Ag for elicitation of delayed-type hypersensitivity in previously immunized mice. This effect was blocked by use of the β2-adrenergic antagonist ICI 118,551 but not by the α-antagonist phentolamine. Local intradermal injection of EPI inhibited the induction of contact hypersensitivity to epicutaneously administered haptens. Surprisingly, injection of EPI at a distant site also suppressed induction of contact hypersensitivity. Thus, catecholamines may have both local and systemic effects. We conclude that specific ARs are expressed on LC and that signaling through these receptors can decrease epidermal immune reactions.

show abstract

“…NE has been shown to activate TH2 cell-dependent antibody response in vivo [9] , and in combination with IL-12, was shown to increase the pool of TH1 cells [16] . In contrast, NE was reported to suppress proliferation of rat peripheral blood T-lymphocytes [17] (which may be related to catecholamine-induced apoptosis [18] ), decrease IL-2 production by murine splenic naïve CD4+ T cells [19] , and inhibit IFN-γ synthesis by PHAstimulated splenic cells [20] . Additionally, A significant suppression of IL-1, IL-2, IL-4, and IFN-γ interferon production by splenic leukocytes, and proliferative response of splenic T lymphocytes following immunization with sheep red blood cells, was observed in the reeler (rl/rl) mice (a neurologic mutant strain with an abnormally high concentration of cerebellar NE) [21] .…”

Section: Discussionmentioning

confidence: 99%

In vitro Activation of Human and Rat Lymphocyte and Macrophage Functions by Norepinephrine

Gómez-Flores¹,

Caballero‐Hernández²,

Weber³

et al. 2005

American J. of Immunology

View full text Add to dashboard Cite

Norepinephrine (NE) has been associated not only with increasing blood pressure, atherosclerosis, heart disease, and other life threatening conditions, but also with altering immune responses by influencing leukocyte functions. In the present study, we evaluated the in vitro effects of NE on rat thymic lymphocyte and human peripheral blood mononuclear cells (HPBMC) functions. We observed that NE marginally, but significantly (P < 0.01) enhanced (1.3-fold increase) proliferation of rat thymic lymphocytes at 10 -5 M, without altering HPBMC proliferation, as compared with untreated control. In addition, NE (10 -5 M) significantly (P < 0.01) enhanced nitric oxide production (2.9 + 0.095 nmol/well) (which reduced 20% cell viability), and stimulated (P < 0.01) TNF-α production (4 + 0.16 pg/ml) by rat macrophages. NE (10 -5 M) was also observed to induce 2-fold increase in mRNA signal of TNF-α, and stimulated that of IL-1 and IL-6 by HPBMC, as compared with untreated control. Taken together, these results indicated that NE was capable to activate in vitro rat and human lymphocyte and macrophage pro-inflammatory response.

show abstract

Cytokine Production by Naive and Primary Effector CD4+ T Cells Exposed to Norepinephrine

Cited by 67 publications

References 42 publications

Sympathetic modulation of immunity: Relevance to disease

Sympathetic modulation of immunity: Relevance to disease

Catecholamines Inhibit the Antigen-Presenting Capability of Epidermal Langerhans Cells

In vitro Activation of Human and Rat Lymphocyte and Macrophage Functions by Norepinephrine

Contact Info

Product

Resources

About