Prostaglandin E1 as a regulator of lymphocyte function

Quagliata, Franco; Lawrence, Victor; Phillips‐Quagliata, Julia M.

doi:10.1016/0008-8749(73)90044-0

Cited by 69 publications

(5 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

724

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

724

120

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“…appears to be an endogenously produced inhibitor of B cell activation. Additional work by Webb's group (15) and others (6)(7)(8)16) implicates PGE2 as well as PGFz, as an inhibitor of B cell function.…”

mentioning

confidence: 99%

Effect of indomethacin in vivo on humoral and cellular immunity in humans

Goodwin¹,

Selinger²,

Messner³

et al. 1978

Infect Immun

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We studied the effect of indomethacin on intradermal skin testing and antibody responses in humans. Since we anI others have shown that prostaglandins are suppressor cell mediators, it was probable that in vivo inhibition of prostaglandin synthesis might enhance the humoral and/or cellular immune response. Administration of indomethacin (Indocin) in a dosage of 100 mg/day to 15 normal men and women resulted in a significantly increased antibody titer to A-Victoria (P < 0.025) as compared with age-and sex-matched controls. There was no difference in titer to ANew Jersey. Since 90% of the subjects had antibody titers to A-Victoria before inoculation, whereas none had detectable titers to ANew Jersey, we interpret this data as suggesting that indomethacin enhances the secondary but not the primary humoral immune response. Indomethacin administration did not alter the intradermal skin test responses.

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“…PGE, also inhibits histamine re lease [29] and has been shown to suppress adjuvant arthritis and the hem agglutinin response to SRBC [31]. More recent evidence indicates that PGE, has a depressing effect on B cells not involved in antibody produc tion [32], Both cholera toxin and PGEi increase cAMP levels by inter acting with adenylate cyclase independent of adrenergic receptors, but cholera toxin requires more time than PGE, to stimulate increased cAMP [29]. Although we found increased cAMP levels and no stimulation of Ig formation with both cholera toxin and PGE" the results of these two compounds differ.…”

Section: Discussionmentioning

confidence: 99%

Effects of Pokeweed Mitogen, Cholera Toxin and Prostaglandin E<sub>1</sub> on Immunoglobulin Production and Cyclic AMP Levels in Tonsillar Lymphocytes

Smith¹,

Sherman²,

Coffey³

1974

Int Arch Allergy Immunol

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Lymphocytes from human tonsils and adenoids and three compounds – pokeweed mitogen (PWM), cholera toxin and prostaglandin E₁ (PGE₁) – were used to study the relationship of immunoglobulin (Ig) synthesis and secretion and intra-cellular levels of cyclic 3′5′-adenosine monophosphate (cAMP). PWM-stimulated lymphocytes synthesized and secreted increased amounts of both IgG and IgA during 120 h of culture, but cAMP levels were not increased during 60 min incubation with PWM. However, both cholera toxin and PGEt significantly increased cAMP levels within 60 min, but did not increase IgG or IgA formation during 72 or 120 h of culture.

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Prostaglandin E1 as a regulator of lymphocyte function

Cited by 69 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.

Effect of indomethacin in vivo on humoral and cellular immunity in humans

Effects of Pokeweed Mitogen, Cholera Toxin and Prostaglandin E<sub>1</sub> on Immunoglobulin Production and Cyclic AMP Levels in Tonsillar Lymphocytes

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