Hemolytic Plaque Formation by Leukocytes in Vitro CONTROL BY VASOACTIVE HORMONES

Melmon, Kenneth L.; Bourne, Henry R.; Weinstein, Yacob; Shearer, Gene M.; Kram, Jerrold; Bauminger, S.

doi:10.1172/jci107530

Cited by 212 publications

(43 citation statements)

References 22 publications

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“…In our experiments when T cells were enriched (and B cells depleted) by passage over plastic bead columns, the inhibition curves of PGE~ and PGE2 on PWM approached the curves of the effects of these compounds on PHA-stimulated cells. There is some evidence in animals that PGs affect B-cell function, but there are no data in man (4,(30)(31)(32)(33). Further investigation of PG effects with other mitogens and on B-cell subpopulations may clarify this issue.…”

Section: Discussionmentioning

confidence: 99%

Suppression of human T-cell mitogenesis by prostaglandin. Existence of a prostaglandin-producing suppressor cell.

Goodwin¹,

Bankhurst²,

Messner³

1977

The Journal of Experimental Medicine

723

120

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Prostaglandins (PGs) I of the E series have been shown to inhibit many in vitro measurements of immune function in experimental animals. These include macrophage inhibitory factor production in guinea pigs (1, 2), direct cytolysis in murine lymphocytes (3), hemolytic plaque formation by murine leukocytes (4), and mitogen-induced stimulation of murine lymphocytes (5). In the human, Lomnitzer et al. (6) have shown that PGEI and PGE2 cause reduction in leukocyte inhibitory factor production by phytohemagglutinin(PHA)-stimulated human lymphocytes. Smith et al. (7) demonstrated significant inhibition of [3H]thymidine incorporation into PHA-stimulated human lymphocytes by PGEI, E2, At, and F~. As in the study by Lomnitzer, the final concentration of PGs was relatively high, I0-~-I0-4M. Ferraris and Derubertis have reported (8) that stimulation of 10 ~ human luekocytes with optimal concentrations of PHA produced -10-8M PGE.These data suggest that PGs of the E series might act as endogenous modulators in human immune reactions. PGEI is produced in the mitogen stimulation of human leukocytes, and may in turn inhibit this stimulation. Thus, data are accumulating to support the hypothesis of Bourne et al. (9) that PGs are important regulators of immune function. One troublesome aspect of the studies on human leukocytes is the great disparity between the amount of PGE produced during mitogen stimulation (~10-SM or 5 ng/ml) and the amount required to suppress mitogen stimulation when added to cultures (~10-5M or 5 pg/ml).In the present paper we describe the effects of lower, more physiologic concentrations of PGs on mitogen stimulation of human lymphocytes and lymphocyte subpopulations. We also describe the effect of PG synthetase inhibitors on mitogen-induced stimulation of these cells. We have identified a population of glass adherent mononuclear cells that suppress T-cell mitogenic activity through production of PGs of the E series.

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Section: Discussionmentioning

confidence: 99%

Suppression of human T-cell mitogenesis by prostaglandin. Existence of a prostaglandin-producing suppressor cell.

Goodwin¹,

Bankhurst²,

Messner³

1977

The Journal of Experimental Medicine

723

120

View full text Add to dashboard Cite

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“…β 2 -AR stimulation has been reported to enhance [220] or inhibit LPS-induced B cell proliferation [195,220] and anti-IgG antibody production [166,220]. Similarly, in vitro Th cell-dependent antibody production increases [220,221] or decreases [13,[222][223][224][225] following β-AR stimulation. These studies suggest that stimulation of β 2 -AR expressed on B cells can either enhance or suppress humoral immunity.…”

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

218

181

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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.

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“…This deficit is overcome by activating B cells in the presence of β2-adrenergic receptor (β2AR) agonists (e.g., terbutaline) (Podojil and Sanders, 2003). However, repeated or prolonged exposure of B cells to NE or other β2AR agonists is immunosuppressive (Melmon et al, 1974;Keller et al, 1983;Maisel, 1994;Harris et al, 1995;Woiciechowsky et al, 1998;Prass et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Impaired antibody synthesis after spinal cord injury is level dependent and is due to sympathetic nervous system dysregulation

Lucin

Sanders

Jones

et al. 2007

Experimental Neurology

169

215

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Individuals with spinal cord injury (SCI) are highly susceptible to infection. This post-traumatic immune suppression is thought to occur via alterations in sympathetic nervous system (SNS) or hypothalamic-pituitary-adrenal (HPA) axis function. Normally, the HPA axis and SNS help coordinate proper immune function. After SCI, the HPA axis becomes activated and descending input to sympathetic preganglionic neurons (SPNs) is impaired. Because lymphoid organs are innervated by SPNs distributed throughout the thoracolumbar spinal cord, we predicted leveldependent immune suppression after SCI due to activation of the HPA axis and loss of descending input to SPNs. We tested this hypothesis by measuring indices of HPA (circulating corticosterone; CORT) and SNS function (norepinephrine (NE) in spleen) as well as antigen-specific antibody synthesis against an exogenous non-self protein following high or low level SCI. Using a midthoracic (T9) spinal contusion injury model, we found that CORT was elevated after SCI with aberrant patterns of diurnal CORT synthesis evident through at least the first 24 hours post-injury. However, splenic NE and antibody synthesis were similar to uninjured controls. Injury severity did not change these parameters. Indeed, CORT, NE and antibody synthesis were similar after T9 contusion or transection SCI. In contrast, high level SCI (T3) caused sustained increases in CORT and splenic NE along with impaired antibody synthesis and elevated splenocyte apoptosis. The immunosuppressive effects of T3 SCI were caused by NE acting at β2-adrenergic receptors (β2AR) and could be reversed using β2AR blockers. Interestingly, impaired antibody after T3 SCI could be Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript mimicked after T9 SCI with a β2AR agonist. These data illustrate the immunosuppressive effects of the SNS after high-level SCI and indicate that immune deficits may be overcome using β-blockers.

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Hemolytic Plaque Formation by Leukocytes in Vitro CONTROL BY VASOACTIVE HORMONES

Cited by 212 publications

References 22 publications

Suppression of human T-cell mitogenesis by prostaglandin. Existence of a prostaglandin-producing suppressor cell.

Suppression of human T-cell mitogenesis by prostaglandin. Existence of a prostaglandin-producing suppressor cell.

Sympathetic modulation of immunity: Relevance to disease

Impaired antibody synthesis after spinal cord injury is level dependent and is due to sympathetic nervous system dysregulation

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