Proliferative response of bovine mononuclear cells to recombinant bovine somatotropin (sometribove)

Bovine mammary gland mononuclear cells (MGMC) and peripheral blood mononuclear cells (PBMC) were isolated during the non‐lactating period to determine if recombinant bovine somatotropin (rbST) enhanced mitogen‐stimulated mononuclear cell proliferation and/or overcame suppressive effects of mammary secretions on mononuclear cell proliferation in vitro. MGMC were hyporesponsive to mitogenic stimulation compared with PBMC. Mammary secretions markedly suppressed the MGMC and PBMC response to mitogens. rbST had no effect on mononuclear cell proliferation in the presence or absence of mitogens. Similarly, rbST did not reverse the suppression of mononuclear cell proliferation by mammary secretions. Under the conditions of this study, rbST had no direct effect on the proliferation of mature bovine mononuclear cells.     

Response of mononuclear cells to recombinant bovine interleukin‐1β during the non‐lactating period

Interleukin‐1 has been shown to play a critical role in the initial stages of lymphocyte proliferation. Recombinant bovine interleukin‐1 may be useful as an immunoenhancer of bovine mammary gland mononuclear cells to enhance resistance of the mammary gland to infection during the non‐lactating period. The objective of this study was to determine if recombinant bovine interleukin‐1β influenced proliferation of blood and mammary gland mononuclear cells obtained during the non‐lactating period. Bovine mononuclear cells were isolated from five primiparous Holstein cows at 14–18 and 28–32 days of involution, and 7–13 days prior to parturition. Proliferation of mononuclear cells in response to recombinant bovine interleukin‐1β was evaluated in the presence and absence of suboptimal concentrations of concanavalin A and pokeweed mitogen. Varying concentrations (0.78–25 ng ml^?1) of recombinant bovine interleukin‐1β did not influence blood or mammary gland mononuclear cell proliferation in the presence or absence of mitogens at any of the time periods studied. Data suggest that exogenous recombinant bovine interleukin‐1β may not be effective as an immunoenhancer of existent mammary gland mononuclear cell populations.     

Enhancement of mammary gland mononuclear cell proliferation by interleukin‐2 in the presence of lactoferrin

The influence of recombinant bovine interleukin‐2 (rBoIL‐2) on mammary gland mononuclear cell proliferation in the presence of lactoferrin and serum albumin was evaluated. Mammary mononuclear cells were isolated from five pregnant Holstein cows during the periparturient period and cultured with 0, 2.5 or 25 ng ml^‐1 of rBoIL‐2. Lactoferrin and serum albumin were evaluated at concentrations ranging from 0 to 2.5 mg ml^‐1. Both 2.5 and 25 ng ml^‐1 of rBoIL‐2 significantly increased mononuclear cell proliferation. Increasing concentrations of lactoferrin resulted in a dose‐dependent reduction of mononuclear cell proliferation in the presence and absence of rBoIL‐2. However, in cells from four of the five cows, rBoIL‐2 treatment (2.5 and 25 ng ml^‐1) resulted in significantly enhanced mononuclear cell proliferation compared to controls (no rBoIL‐2) even in the presence of the highest concentration of lactoferrin. Serum albumin had little influence on mononuclear cell proliferation. Results of this study suggest that lactoferrin inhibits mammary gland mononuclear cell proliferation, and that rBoIL‐2 can overcome lactoferrin‐induced hyporesponsiveness.     

Bimodal effects of lactoferrin on proliferation of an interleukin‐2‐dependent cytotoxic t‐lymphocyte cell line

The mechanism for the hypo‐responsiveness of mammary gland mononuclear cells (MGMCs) to mitogen stimulation is poorly understood. It has been hypothesized that hypo‐responsiveness of MGMCs may be due to interference by lactoferrin or other whey proteins present in mammary secretions with lymphocyte proliferation stimulated by interleukin‐2 (IL‐2). To address this hypothesis, an experiment was designed to evaluate proliferation of an IL‐2‐dependent bovine cytotoxic T‐lymphocyte cell line (BT‐2) in the presence of apo‐ and iron‐saturated lactoferrin (APOLF and FELF) and transferrin (APOTF and FETF), immunoglobulin G (IgG) and serum albumin (SA) at concentrations ranging from 0.02 to 2.5 mg ml^‐1. The lowest concentration of APOLF and FELF increased BT‐2 cell proliferation. Conversely, increasing concentrations of LF significantly inhibited BT‐2 cell proliferation. Only the highest concentrations of APOTF, FETF and IgG negatively influenced BT‐2 cell proliferation. Serum albumin had no effect. These data suggest that LF has a dose‐dependent bimodal influence on a bovine IL‐2‐dependent cytotoxic T‐lymphocyte cell line, and high concentrations of LF and other mammary secretion whey proteins may be associated with MGMC hypo‐responsiveness during the non‐lactating period, possibly through interference with IL‐2‐stimulated lymphocyte proliferation.     

Lack of immunosuppression by ketoconazole and itraconazole.

The antifungal drugs ketoconazole and itraconazole were evaluated for their effects in the following test systems: in vitro, phytohaemagglutinin (PHA)-induced proliferation of human peripheral blood mononuclear cells and IL-2-driven proliferation of CTLL-2 cells; in vivo, antibody response to sheep red blood cells (SRBC) and delayed-type hypersensitivity (DTH) reaction to oxazolone. At a concentration of 10 microM, ketoconazole moderately and itraconazole strongly inhibited thymidine (Thd) incorporation in human peripheral blood mononuclear cells cultured in medium supplemented with 5% human serum. Increasing the serum concentration from 5 to 20% almost completely reversed these inhibitory effects. Also, cell viability, found to be less than 15% in cultures containing 10 microM itraconazole was restored by increasing the serum concentrations in the culture medium. Similar observations were made in experiments using IL-2-stimulated CTLL-2 cells: the growth inhibition in the presence of 10 microM ketoconazole or 1 microM itraconazole could be counteracted by increased serum supplementation. In vivo, subchronic intraperitoneal dosing with 40 mg/kg ketoconazole or itraconazole to mice had no effect on the antibody response to SRBC as measured by the number of splenic IgM and IgG plaque-forming cells and did not significantly affect the DTH response to oxazolone. These data indicate that neither ketoconazole nor itraconazole exert immunosuppressive properties in vivo. Their in vitro inhibitory effects on PHA-induced lymphocyte proliferation and IL-2-dependent CTLL-2 growth are reversed by the serum supplementation to the culture medium and these activities should therefore be considered as in vitro artefacts.     

白细胞介素-2对培养的乳腺癌细胞Bcap-37增殖的促进作用

目的 :研究白细胞介素 2 (IL 2 )对人乳腺癌Bcap 37细胞系增殖的影响 ,并探讨其可能的机制。方法 :以培养的Bcap 37细胞进行了以下实验 :用MTT比色法 ,测定IL 2对该细胞增殖的剂量效应 ;用免疫组化染色法 ,检测其表面IL 2的表达 ;用RT PCR技术 ,检测该细胞中IL 2Rα、β和γmRNA的表达 ;用流式细胞术 ,观察IL 2对该细胞细胞周期各阶段DNA含量的影响 ;用激光扫描共聚焦显微镜技术 ,检测IL 2对该细胞内Ca2 + 水平的影响。结果 :IL 2 (1× 10 5～ 1× 10 6U/L)可显著促进乳腺癌细胞Bcap 37的增殖。培养的Bcap 37细胞可分泌IL 2并表达IL 2Rα、β和γ。用流式细胞仪检测Bcap 37细胞中DNA的含量发现 ,IL 2 (1× 10 5U/L)可提高该细胞由G1期进入G2 和S期的比例。激光共聚焦法检测到IL 2 (1× 10 5U/L)可使Bcap 37细胞内的Ca2 + 浓度降低。结论 :IL 2参与了对乳腺癌细胞增殖的调节 ,其促增殖作用与该细胞上IL 2受体的表达 ,细胞中DNA含量的变化和Ca2 + 浓度的降低有关。     

Enhancement of bovine mammary gland mononuclear cell Mitogenesis by recombinant bovine interleukin‐2

Recombinant bovine interleukin‐2 was evaluated as a potential immunoenhancer of bovine mammary gland mononuclear cells. Bovine mononuclear cells were isolated from five primiparous Holstein cows at 14–18 and 28–32 days of involution and at 7–13 days prior to parturition. Optimal stimulatory concentrations of the T‐lymphocyte mitogen concanavalin A and the T‐dependent B‐lymphocyte mitogen pokeweed mitogen were determined to be 6.25 and 2 μg ml^‐1 respectively. Proliferation of mononuclear cells in response to recombinant bovine interleukin‐2 was evaluated in the presence of suboptimal concentrations of concanavalin A and pokeweed mitogen to avoid masking potential effects of recombinant IL‐2. Bovine blood and mammary gland mononuclear cells were highly responsive to mitogens and to recombinant bovine interleukin‐2. The response of mammary gland mononuclear cells to recombinant bovine interleukin‐2 was comparable with the response of blood mononuclear cells. The data suggest that recombinant bovine interleukin‐2 may be an effective in vivo immunoenhancer of mammary gland mononuclear cells.     

Amniotic membrane is an immunosuppressor of peripheral blood mononuclear cells

Amniotic membrane (AM) is the inner layer of the placenta, which is in contact with the fetus; it has been used for transplantation in ocular surface diseases. It has been reported that amniotic membrane promotes epithelialization, inhibits angiogenesis and diminishes ocular inflammation. A persistent epithelial defect is the delay in epithelial wound healing caused by infiltrating inflammatory cells into the cornea and amniotic membrane transplantation has been successfully used in its treatment, however the mechanism of action in inhibiting inflammation it is not well understood. This study was aimed at determining whether denuded amniotic membrane (dAM) induces anti-inflammatory effects on peripheral blood mononuclear cells. Methods: Human peripheral blood mononuclear cells (PBMC) were cultured on dAM. Proliferation and apoptosis assays were performed on PBMC; and synthesis and secretion of pro-inflammatory cytokines by these cells was analyzed. Results: dAM induced apoptosis and inhibited cell proliferation of PBMC; and abolished the synthesis and the secretion of pro-inflammatory cytokines even when they were LPS stimulated. In contrast, when PBMC were cultured on hydrophilic membrane cell culture inserts, apoptosis was not significantly induced, cell proliferation was conserved, and synthesis and secretion of pro-inflammatory cytokines were not affected. Conclusions: Taken together, these results could explain the anti-inflammatory in vivo effects observed when the amniotic membrane is used as a transplant.     

Interleukin 2-independent stimulation of rabbit chondrocyte collagenase and prostaglandin E2 production by an interleukin 1-like factor

In the present study, interleukin 1 (IL 1)-containing media from different sources, namely a murine macrophage cell line (P388D1), rabbit peritoneal macrophages, and human peripheral blood mononuclear cells, were compared for their effect on thymocyte proliferation and on collagenase and PGE2 secretion by chondrocytes. A high correlation was found between the enhancement of thymocyte proliferation and the induction of collagenase and PGE2 secretion by chondrocytes. Furthermore, a highly purified IL 1-like factor, namely mononuclear cell factor (MCF) was also active on chondrocytes. The addition of highly purified IL 2 to rabbit chondrocytes had no effect on collagenase and PGE2 secretion induced by IL 1-containing media. Our findings suggest that the factor which induced collagenase and PGE2 secretion by rabbit chondrocytes was an IL 1-like factor. Thus, collagenase secretion by chondrocytes may be used as an IL 2-insensitive assay for the detection of IL 1-like factors.     

不同类型乳腺增生性疾病患者心理健康的比较

目的 探讨不同类型乳腺增生性疾病患者的心理健康状况.方法 应用HP Agilent IMAGE POINTHX彩超仪,诊断和区分单纯性乳腺增生症(研究1组)、乳腺囊性增生病(研究2组)和健康妇女各60例,在月经周期的月经期、增生期、分泌期、月经前期采用SCL-90评定精神状态.结果 两研究组在月经期和月经前期躯体化、人际敏感、抑郁、焦虑等因子分比健康对照组高;在增生期两研究组抑郁、焦虑等因子分比健康对照组高,研究l组的躯体化因子分比健康对照组高;在分泌期两研究组躯体化、抑郁、焦虑等因子分比健康对照组高;月经期研究1组躯体化、焦虑因子分及月经前期焦虑因子分比研究2组高,有显著性差异(P＜0.05),其他因子两组问差异不显著.结论 乳腺增生性疾病患者心理健康状况较健康妇女差,主要表现为躯体化、人际敏感、抑郁、焦虑,并随月经周期而变化,而且单纯性乳腺增生症患者心理健康状况较乳腺囊性增生病患者更差.     

Protein synthesis and secretion by activated human lymphocytes.

Human peripheral blood mononuclear cells showed increased synthesis and secretion of protein in response to stimulation by mitogens. Protein secretion in response to concanavalin A (Con A) correlated with cellular proliferation and originated from the proliferating cells. Selective depletion of either B lymphocytes or monocytes did not lead to a reduction in the total protein secreted, suggesting that the T lymphocyte was the cell contributing most of the synthetic activity. It is concluded that the measurement of newly synthesized and secreted protein by Con A activated mononuclear cells is a measurement of the T-lymphocyte response.     

Determination of interleukin-5 secretion from drug-specific activated ex vivo peripheral blood mononuclear cells as a test system for the in vitro detection of drug sensitization

BACKGROUND: In vitro detection of drug sensitization is still limited. The lymphocyte transformation test, which determines drug-specific proliferation, is the only in vitro test for detecting drug sensitization at the cellular level irrespective of the reaction's clinical phenotype. Accumulation of eosinophils following IL-5 secretion from drug-specific stimulated T cells is a characteristic histological feature of drug-induced skin eruptions. OBJECTIVE: We determined whether in vitro drug-specific activation of ex vivo peripheral blood mononuclear cells from 10 patients with drug-induced maculopapular exanthems and three patients with severe skin reactions results in secretion of IL-5, IL-10 or IFN-gamma and assessed the sensitivity and specificity of drug-specific IL-5 secretion as a test system compared with the lymphocyte transformation test and patch tests. Furthermore, the subsets of CD4+ and CD8+ T cells involved in drug-specific proliferation, IL-5 secretion and mRNA expression were examined in three patients. METHODS: Drug-specific proliferation of peripheral blood mononuclear cells in the lymphocyte transformation test was investigated by 3H-thymidine uptake, and culture supernatants taken after 5 days were analysed for IL-5, IL-10 and IFN-gamma concentrations by ELISA technique. IL-5 mRNA expression was determined by RT-PCR. RESULTS: Drug-specific activation of peripheral blood mononuclear cells consistently resulted in IL-5 and to a lesser extent in IL-10 and IFN-gamma secretion. The sensitivities of the patch test, lymphocyte transformation test and assessment of drug-specific IL-5 secretion for the detection of drug sensitization were 55%, 75% and 92%, respectively. CONCLUSION: These data suggest a role for the determination of drug-specific IL-5 secretion by ex vivo peripheral blood mononuclear cells for the in vitro detection of drug-sensitization in drug-induced maculopapular exanthems.     

Infliximab Inhibits Activation and Effector Functions of Peripheral Blood T Cells in vitro from Patients with Clinically Active Ulcerative Colitis

Many patients with inflammatory bowel disease (IBD) are undergoing therapy with infliximab, an antibody specific for TNF. However, the exact mechanisms of action of infliximab are not completely understood. The aim of this study was to determine the in vitro effects of infliximab on blood T cells derived from anti‐TNF therapy–naïve ulcerative colitis (UC) patients with clinically active disease. Peripheral blood mononuclear cells were stimulated polyclonally or by antigen in the presence or absence of infliximab. The T cell phenotype was investigated by flow cytometry, cytokine secretion was determined by ELISA, and cell proliferation was determined by thymidine assay or CFSE dye. Presence of infliximab resulted in reduced expression of CD25 in CD4⁺ and CD8⁺ T cell populations and inhibited secretion of IFN‐γ, IL‐13, IL‐17A, TNF as well as granzyme A. Infliximab also suppressed CD4⁺ and CD8⁺ T cell proliferation. These effects of infliximab were recorded both in T cells activated by polyclonal and antigen‐specific stimulation. The effects of infliximab on T cell apoptosis and induction of FOXP3⁺CD4⁺ T regulatory cells were ambiguous and depended on the originating cellular source and/or the stimulation mode and strength. In conclusion, infliximab is able to reduce T cell activation as measured by CD25, proliferation and cytokine secretion in vitro from UC patients with clinically active disease. These data suggest that suppression of T cell activity may be important for infliximab‐mediated disease remission in patients with UC.     

Influence of serum from healthy or breast tumor-bearing women on the growth of MCF-7 human breast cancer cells

Sera from women healthy (HW) or with breast (BCW), ovarian or endometrial cancer, were added (10%) to the culture media of MCF-7 cells and cell proliferation assessed 4 days later to verify: a) whether sera from BCW, obtained before or 8 days after tumor ablaction, influence the proliferation of these cells, b) whether the effects of serum from BCW are specific for mammary tumor cells. Sera from BCW, but not sera from women with ovarian or endometrial cancer, increased MCF-7 cell proliferation in comparison with sera from HW. After surgical ablation of the breast tumors, serum's ability to increase MCF-7 cell proliferation decreased significantly. These effects cannot be explained by differences on serum levels of estradiol or melatonin. These results suggest the presence of growth-promoting substances of possible tumoral origin in serum of BCW, a fact that should be considered as support for the surgical treatment of tumor masses.     

Evidence to suggest that the phosphodiesterase 4 isoenzyme is present and involved in the proliferation of umbilical cord blood mononuclear cells

BACKGROUND: The type 4 phosphodiesterase (PDE) isoenzyme is the main isoenzyme of PDE involved in the control of adult mononuclear cell proliferation. OBJECTIVE: To establish whether PDE isoenzymes are present in umbilical cord blood mononuclear cells by the use of selective PDE inhibitors, and to identify which PDE isoenzymes are involved in controlling the proliferation of cord blood mononuclear cells. METHODS: Cord blood was obtained from normal deliveries and mononuclear cells isolated as described previously [1] with some modifications. Mononuclear cells were then stimulated to proliferate with phytohaemagglutinin (PHA) (2 microg/mL) in the presence of selective PDE inhibitors. Proliferation was measured by [3H]-thymidine incorporation. RESULTS: The type 4 PDE inhibitors (CDP840, rolipram and RO 20-1724), and the mixed PDE3/4 inhibitor, zardaverine, produced a concentration-related inhibition of PHA-stimulated cord blood mononuclear cell proliferation (P < 0.05, ANOVA). The non-selective PDE inhibitor, theophylline, also produced a concentration-related inhibition of proliferation (P < 0.05, ANOVA). In contrast, the PDE1 inhibitor, vinpocetine, the PDE3 inhibitor, siguazodan, and the PDE5 inhibitor, zaprinast, were unable to inhibit cord blood mononuclear cell proliferation. CONCLUSION: PDE4 is present in umbilical cord mononuclear cells and is involved in the control of cord blood mononuclear cell proliferation.     

Functional consequences of cyclin D1 overexpression in human mammary luminal epithelial cells

The proliferation of eukaryotic cells is primarily regulated by a decision made during the G1 phase of the cell cycle as to remain in the cycle and divide, or to withdraw from the cycle and adopt a different cell fate. During this time, environmental signals, which regulate the synthesis of the G1 cyclins, are coupled to cell division. In this context, mammalian D-type cyclins have been shown to control progression through the G1 phase of the mammalian cell cycle. Specifically, cyclin D1 has been reported frequently to be amplified, over-transcribed and overexpressed in human breast carcinomas. Although the effects of cyclin D1 overexpression have been examined in human breast carcinoma cell lines, the biological consequences of cyclin D1 expression in normal human mammary epithelial cells remain to be elucidated. In this study we have stably over expressed cyclin D1 in human mammary luminal epithelial cells in order to more directly address the role of cyclin D1 in cell cycle control and tumorigenesis of the human breast. Here, we demonstrate that the effect of cyclin D1 overexpression in these cells is to reduce their growth factor dependency, as well as shorten the duration of G1 and correspondingly reduce the mean generation time. Collectively, our data indicate that deregulation of cyclin D1 expression in human mammary epithelial cells can provide a growth advantage and hence contribute to the oncogenic potential of these cells.     

Differential effects of AKT1(p.E17K) expression on human mammary luminal epithelial and myoepithelial cells

Recently, we identified a somatic mutation in AKT1, which results in a glutamic acid to lysine substitution (p.Glu17Lys or E17K). E17K mutations appear almost exclusively in breast cancers of luminal origin. Cellular models involving cell lines such as human mammary epithelial and MCF10 are model systems that upon transformation lead to rare forms of human breast cancer. Hence, we studied the effects of E17K using a clinically pertinent luminal cell line model while providing evidence to explain why E17K mutations do not occur in the mammary myoepithelium. Thus the purpose of our study was to perform a functional and differential proteomics study to assess the role of AKT1(E17K) in the development of breast cancer. We used a set of genetically matched nontumorigenic and tumorigenic mammary luminal and myoepithelial cells. We demonstrated that in myoepithelial cells, expression of E17K inhibited growth, migration, and protein synthesis compared with wild-type AKT1. In luminal cells, E17K enhanced cell survival and migration, possibly offering a selective advantage in this type of cell. However, antineoplastic effects of E17K in luminal cells, such as inhibition of growth and protein synthesis, may ultimately be associated with favorable prognosis. Our study illustrates the importance of cellular context in determining phenotypic effects of putative oncogenic mutations.     

Spontaneous secretion of interleukin-4, interleukin-10 and interferon-gamma by first trimester decidual mononuclear cells

PROBLEM: A T-helper cell type 2 (Th2) cytokine dominated microenvironment has been predicted to be crucial for successful pregnancy. However, little information is available about local cytokine secretion in the human decidua. We determined the spontaneous secretion of interleukin-4 (IL-4), interferon-gamma (IFN-gamma) and IL-10 by decidual mononuclear cells at the single cell level and compared it with their secretion by peripheral blood mononuclear cells (PBMC) in the first trimester of pregnancy. METHODS OF STUDY: The cytokine secretion from decidual and blood cells was detected by a sensitive enzyme-linked immunosorbent spot-forming cell (ELISPOT)-assay. RESULTS: Cells secreting IL-4 (median 153, range 8-530), IL-10 (median 188, range 32-1600) and IFN-gamma (median 123, range 15-1140) were detected in all decidual and blood samples. The cytokine secretion showed a co-linear pattern in both the blood and decidua, i.e. when one cytokine was secreted at high levels, the others followed the trend. No correlation was found between the number of cytokine secreting cells in blood and decidua for any of the cytokines. CONCLUSIONS: Interleukin-4 and IL-10 are locally secreted in the decidua early during normal pregnancy, probably counteracting the fetal rejecting effects of co-expressed IFN-gamma. The cytokine secretion by blood cells does not generally reflect the local secretion pattern during first trimester pregnancy.     

T Cell-Mediated Production of Tumour Necrosis Factor-α by Monocytes

The aim of this study was to examine the tumour necrosis factor (TNF)-alpha production by peripheral blood mononuclear cells activated by mitogens. Considerable amounts of TNF-alpha, ranging from 1.0 to 5.0 ng/ml, were present in the supernatants of cultures of human peripheral blood mononuclear cells (PBMC), stimulated with either the anti-CD3 monoclonal antibody OKT3 or the lectin phytohaemagglutinin (PHA). The amount of TNF-alpha secreted in the supernatant was closely correlated to the degree of T cell proliferation in such cultures, as measured by [3H]TdR incorporation. In the absence of proliferating T cells the mitogens did not induce secretion of TNF-alpha by monocytes. Supernatants of proliferating T cells were shown to induce TNF-alpha production by monocytes. The macrophage-activating factor gamma interferon (IFN-gamma) was also shown to induce, in the absence of endotoxin, TNF-alpha secretion by monocytes in a dose-dependent manner. The induction of TNF-alpha production by supernatants of proliferating T cells could largely be abrogated by passaging the supernatants on an anti-IFN-gamma column before adding them to the monocytes. It is therefore concluded from this study that the production of TNF-alpha by monocytes can be induced by proliferating T cells and that this induction can largely be attributed to the T cell lymphokine IFN-gamma.     

Accessory cell function of human alveolar macrophages in B-cell activation induced by pokeweed mitogen

The effect of alveolar macrophages (AM) on pokeweed mitogen (PWM)-stimulated immunoglobulin (Ig) secretion by unfractionated and monocyte-depleted human peripheral blood mononuclear cells was studied. Responsiveness in monocyte-depleted peripheral blood mononuclear cell populations could be partially restored by addition of autologous monocytes and to a lesser extent with AM. Addition of AM to unfractionated peripheral blood mononuclear cells resulted in significant inhibition of Ig secretion, especially at high (5-10 micrograms/ml) doses of PWM. The degree of suppression was proportional to the number of AM present. On the other hand, addition of monocytes to similar unfractionated peripheral blood mononuclear cell cultures did not result in suppression of Ig secretion at any of the doses of PWM used. Suppression by AM was not attributable to an alteration of response kinetics. The results demonstrate that mononuclear phagocytic cells are necessary for activation of polyclonal Ig secretion by human B cells and that AM are capable of suppressing this response.