Subversion of immune system by tumor cells and role of prostaglandins.

Plescia, Otto J.; Smith, Allan H.; Grinwich, Kazimiera D.

doi:10.1073/pnas.72.5.1848

Cited by 284 publications

(86 citation statements)

References 11 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: 92%

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: 92%

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

View full text Add to dashboard Cite

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“…Prostaglandin E 2 (PGE 2 ) directly suppresses various immune cells such as macrophages, neutrophils, Th1, CTL and NK cells, while it promotes Th2, Th17 and regulatory T cell responses as well as the development of tumor-associated suppressive macrophages [93,[100][101][102][103]. The Th17-promoting activity of PGE 2 is related to its ability to suppress the production of the Th17-inhibitory IL-12, while enhancing the Th17-supporting IL-23 secretion by dendritic cells [104].…”

Section: Pgementioning

confidence: 99%

“…In line with the immunosuppressive, tumor promoting function of PGE 2 , inhibitors of prostaglandin synthesis, such as indomethacin and aspirin, have been shown to inhibit tumor growth [101] and restore anti-tumor activity by altering the balance between IL-10 and IL-12 [119]. Recently, this issue has reached a renaissance where specific COX2 inhibitors have been proposed to be potential drugs for tumor prevention [120].…”

Section: Pgementioning

confidence: 99%

The Multifaceted Roles Neutrophils Play in the Tumor Microenvironment

Sionov

Fridlender

Granot

2014

Cancer Microenvironment

342

261

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Neutrophils are myeloid cells that constitute 50-70 % of all white blood cells in the human circulation. Traditionally, neutrophils are viewed as the first line of defense against infections and as a major component of the inflammatory process. In addition, accumulating evidence suggest that neutrophils may also play a key role in multiple aspects of cancer biology. The possible involvement of neutrophils in cancer prevention and promotion was already suggested more than half a century ago, however, despite being the major component of the immune system, their contribution has often been overshadowed by other immune components such as lymphocytes and macrophages. Neutrophils seem to have conflicting functions in cancer and can be classified into anti-tumor (N1) and pro-tumor (N2) sub-populations. The aim of this review is to discuss the varying nature of neutrophil function in the cancer microenvironment with a specific emphasis on the mechanisms that regulate neutrophil mobilization, recruitment and activation.

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“…Prostaglandins are important regulatory factors of epithelial cell function and, under certain circumstances, prostaglandins can stimulate cell proliferation and suppress immune response to neoplastic cells (Plescia et al, 1975). In addition, several groups have shown that high concentrations of free arachidonic acid can promote apoptosis, independently of prostaglandin formation (Surette et al, 1996;Chan et al, 1998;Longo et al, 1999).…”

Section: Epidemiologymentioning

confidence: 99%

Aspirin and lung cancer in women

et al. 2002

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The association between aspirin use and lung cancer risk in women was examined in a case -control study nested in the New York University Women's Health Study, a large cohort in New York. Case subjects were all the 81 incident lung cancer cases who had provided information about aspirin use at enrollment and during the 1994 -1996 follow up. Ten controls per case were randomly selected from among study participants who matched a case by age, menopausal status, and dates of enrollment and follow-up. Relative to no aspirin use, the odds ratio for lung cancer (all histological sub-types combined) among subjects who reported aspirin use three or more times per week for at least 6 months was 0.66 (95% confidence interval 0.34 -1.28), after adjustment for smoking and education. A stronger inverse association was observed in analyses restricted to non-small cell lung cancer (adjusted odds ratio 0.39, 95% confidence interval 0.16 -0.96). These results suggest that regular aspirin use might be inversely associated with risk of lung cancer in women, particularly the non-small cell sub-type. British Journal of Cancer (2002) A role for nonsteroidal anti-inflammatory drugs (NSAIDs) in preventing lung carcinogenesis is suggested by animal models, in which aspirin and other NSAIDs inhibited the formation of chemically-induced lung tumours (Jalbert and Castonguay, 1992;Castonguay et al, 1998;Rioux and Castonguay, 1998).The relation between NSAIDs use and lung cancer has been examined in at least six epidemiological studies published to date. In a trial of aspirin among British physicians, there were fewer lung cancer deaths among aspirin users compared with nonusers (Peto et al, 1988). In two prospective studies, no overall association was observed between aspirin use and lung cancer, although when stratified by gender, regular aspirin use appeared to be inversely associated with lung cancer incidence (Paganini-Hill et al, 1989) and mortality (Thun et al, 1993) in women. In a prospective study based on the first National Health and Nutrition Examination Survey, self-reported use of aspirin during the 30-day period preceding a subject's recruitment into the cohort was associated with a significant reduction in lung cancer incidence compared with nonuse (Schreinemachers and Everson, 1994). Two case -control studies found no significant associations between aspirin use and risk of lung cancer (Rosenberg, 1995;Langman et al, 2000).To assess further the potential effect of aspirin use on lung cancer risk, we analysed the data in a case -control study of lung cancer nested in the New York University (NYU) Women's Health Study cohort. MATERIALS AND METHODS Study populationThe NYU Women's Health Study is a long-term prospective cohort study that has been described in detail elsewhere (Toniolo et al, 1991, 1995). Briefly, between March 1985 and June 1991 mostly Caucasian women between ages of 31 and 70 years were enrolled at a mammography screening clinic in New York City. Women, who in the preceding 6 months had neither used hormonal m...

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Subversion of immune system by tumor cells and role of prostaglandins.

Cited by 284 publications

References 11 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.

The Multifaceted Roles Neutrophils Play in the Tumor Microenvironment

Aspirin and lung cancer in women

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