Unseparated Mononuclear Cells Research Articles

Antigen-specific immunosuppression in visceral leishmaniasis is cell mediated.

Visceral leishmaniasis is associated with an antigen-specific immunosuppression during the acute disease. Patients become responsive to Leishmania antigen in both in vivo and in vitro assays after successful antimony therapy. The cell type involved in the suppression of lymphocyte reactivity to Leishmania antigen was studied by selective depletion of mononuclear cell (MNC) populations and in co-cultivation experiments. Adherent cells were depleted on plastic and by passage on nylon wool columns. High-avidity Fc+ cells were depleted by adherence to BSA-anti-BSA complexes and OKT4+ and OKT8+ cells were depleted by treatment with monoclonal antibody (anti-OKT4+ and OKT8+) and complement. Depletion of MNC preparations of adherent cells, high-avidity Fc+ cells, OKT4+ cells and OKT8+ cells failed to restore the lymphocyte reactivity to Leishmania antigen. Antimony therapy was associated with restoration of the proliferative responses of unseparated MNC (before treatment 460 +/- 76 cpm and after treatment 4,293 +/- 1,442 cpm). Co-culture of frozen cells obtained before chemotherapy with autologous MNC obtained after treatment reduced the response of posttreatment cells to Leishmania antigen by 80%. We conclude that the antigenic specific suppression of lymphocyte proliferation in visceral leishmaniasis is cell mediated.

The Functional Deficiency of B Lymphocytes in Patients with Lung Cancer is Due to Inadequate T-Cell Help and Excessive Suppression by T and Non-T Cells

The proliferative and plaque-forming cell (PFC) responses of unseparated mononuclear cells (MNC) and B- and T-cell-enriched populations of cells were analyzed in 15 patients with lung cancer to determine the mechanisms involved in the functional abnormality of their B cells. The PFC responses of the MNC of the patient group were significantly lower than those of normal controls. In addition, the enriched B cells of several patients showed a further decrease in their PFC responses after coculture with autologous T cells compared with their respective MNC responses. The proliferative response against phytohemagglutinin (PHA) was also lower in many of the patients after similar cocultures. Cocultures of patients' B cells with T cells from normal controls significantly enhanced the PFC responses in 7 patients. In most of the normal controls, B lymphocytes showed a significant decrease in their PFC responses after coculture with the patients' T cells. Although the percentages of total T cells, T-helper, and B cells were within the normal range, the number of suppressor T cells was significantly higher in the patient group. These results indicate that a combination of insufficient T-cell help, excessive suppression by both T and non-T cells, and a possible intrinsic B-cell abnormality are responsible for the B-cell functional deficiency observed in patients with lung cancer.

Use of OKT3 hybridoma cells to clonally activate CD3 + human T lymphocytes

A simple and reliable method was developed to induce clonal growth of resting human T cells. In this limiting dilution (LD) culture system, responder cells (unseparated mononuclear cells, E rosette-purified T cells, or cell sorter-separated CD4 + and CD8 + subsets) were activated by irradiated anti-CD3-secreting (OKT3) hybridoma cells in the presence of exogenous IL-2 (crude culture supernatant or recombinant IL-2). Under these conditions, one out of 2–3 CD4 + and CD8 + T celll developed into a proliferating cell clone. Addition of recombinant IL-1 slightly enhanced the growth frequency and increased the clone size of CD4 + cells but did not affect the growth pattern of CD8 + cells.

Vaccination-induced activation of human blood T cells suppressing pneumococcal polysaccharide-specific B cells.

In order to study the regulation of the human B cell response to pneumococcal polysaccharides (PPS), anti-PPS-secreting cells (SC) and Ig-SC were quantitated in unstimulated and EBV-stimulated cultures of blood mononuclear cells (MNC) established before and one and two weeks after vaccination. In unstimulated cultures established one week after vaccination, significant numbers of anti-PPS-SC were detected; however, they were observed only in cultures depleted of T cells (mean: 62/10(6)), suggesting the presence of T cells suppressing in vivo-activated PPS-specific B cells. In EBV-stimulated cultures depleted of T cells, low numbers of anti-PPS-SC were observed before the vaccination, and the numbers of these cells increased significantly two weeks after the immunization (from 28 to 48/10(6)). In contrast, the numbers of anti-PPS-SC and total Ig-SC decreased in EBV-stimulated cultures of unseparated MNC established after the vaccination, suggesting T cell-mediated suppression. The findings were not explained by changes in the numbers of blood T helper (Leu 3+) or T suppressor (Leu 2+) cells following the vaccination. Possibly the vaccination induces the appearance in the blood of activated suppressor cells responsible for the suppression of B cells in unstimulated and EBV-stimulated cultures.

Modulation of lymphocyte proliferation and immunoglobulin synthesis by interferon-γ and “type I” interferons

Interferon (IFN)-α and IFN-β (“type I” IFNs), but not IFN-γ reduced phytohemagglutininor pokeweed mitogen (PWM)-induced proliferation in cultures of human mononuclear leukocytes. Proliferation induced by specific antigens (tuberculin PPD or tetanus toxoid) or by exogenous interleukin 2 (IL-2) was strongly inhibited by type I IFNs and, to a lesser extent, by IFN-γ as well. Inhibition of proliferation in mitogen-stimulated cultures was not due to a reduced production of IL-2 or to an inhibition of IL-2 receptor expression. Type I IFNs inhibited immunoglobulin (Ig) production in PWM-stimulated unseparated mononuclear cells, whereas IFN-γ enhanced Ig production in such cultures. In cultures of purified B cells type I IFNs caused a stimulation of Ig production and this B-cell differentiation factor (BCDF) hike activity of IFNs was synergistically enhanced in the presence of IL-2. IFN-γ produced less BCDF-like activity than type I IFNs. These results show that in some instances type I IFNs can be more potent in affecting functions of cells of the immune system than IFN-γ.

Sister chromatid exchange in highly purified human B and T lymphocytes.

Sister chromatid exchange (SCE) rates were determined in human peripheral blood B and T lymphocyte populations highly purified by immunologic methods. The purified populations were supplemented with gamma-irradiated unseparated autologous mononuclear cells to restore helper-functions and stimulated with pokeweed mitogen (PWM) and phytohemagglutinin (PHA), respectively. Measured at the different peaks of proliferation after identical bromodeoxyuridine (BrdU) incubation times, T lymphocytes showed significantly higher SCE frequencies than B lymphocytes. In both populations, different proliferation kinetics and a different minimal BrdU concentration for sister chromatid differentiation (SCD) were observed.

Evaluation of the interaction of mononuclear phagocytes with ovarian carcinoma cells in a colony assay.

The effect of human peripheral blood monocytes on the SW626 ovarian carcinoma line was investigated in a colony assay in agar, Percoll-enriched monocytes inhibited colony formation by SW626 carcinoma cells at effector-to-target cell (E:T) ratios as low as 0.3:1. In contrast the same effectors had little cytolytic effect in a 48 h thymidine-release assay at E:T ratios as high as 40:1. Monocyte-depleted nonadherent cells had little inhibitory capacity on SW626 colony formation, whereas unseparated mononuclear cells were intermediate between Percoll-enriched monocytes and lymphoid cells. Sorting of cells positive for the monoclonal antibody marker MO2 confirmed the monocytic nature of cells which inhibited colony formation. Ovarian carcinoma cells freshly isolated from 9 patients were heterogenous in their susceptibility to colony inhibition by mononuclear phagocytes. Cells from 4 patients were not inhibited by effector cells and in one subject promotion of colony formation by mononuclear phagocytes was observed. With 4 cell preparations inhibition of colony formation was found as with the SW626 line. Colony assays may provide a useful methodological approach, particularly when effector cells mediate low levels of killing, of doubtful biological significance, in conventional isotope release assays, or when growth promotion is to be evaluated.

45] Parasiticidal activity of macrophages against Plasmodium

This chapter describes methods for activating macrophages that enhances the phagocytosis and killing of intraerythrocytic parasites. It also discusses phagocytic and cytotoxicity assays using agents that are infectious for both humans and rodents. Macrophages are activated in vivo by infection of mice with either bacillus Calmette–Guerin (BCG) or with malaria parasites. In addition, macrophages may also be activated in vitro by the infection of mice with malaria. Lymphokines (LK) may be prepared from BCG-infected mice and from malaria-infected mice. Malarial antigen is prepared from parasitized erythrocytes (PE) that are enriched by the centrifugation of erythrocytes in Dulbecco's modified Eagle's medium (DMEM) at 750 g for 10 minutes. LK may also be prepared from concanavalin A (Con A)-stimulated human mononuclear cells by cultivating unseparated mononuclear cells with Con A in RPMI 1640 supplemented with 7.5% human serum, penicillin, and streptomycin and 50 μM mercaptoethanol at 37°. Rodent malaria parasites are maintained by blood passage in mice. Parasitemias are determined on Giemsa-stained blood films. Blood is obtained in heparin, the number of red cells counted, and a fixed number of parasites injected into mice.

Cytotoxic lymphokines produced by cloned human cytotoxic T lymphocytes. I. Cytotoxins produced by antigen-specific and natural killer-like CTL are dissimilar to classical lymphotoxins.

Several cloned lines of IL 2-dependent human T cells derived from alloantigen, mitogen, or IL 2-stimulated peripheral blood lymphocytes were examined for their surface marker expression, cytolytic activity in a 51Cr-release assay, and capacity to release cytotoxic lymphokines. Thirty cell lines exhibiting either antigen-specific natural killer cell activity or lectin-dependent killer cell function, which expressed either the CD4 or CD8 surface differentiation markers, were capable of producing cytotoxin(s) in response to the lectins phytohemagglutinin and concanavalin A. Cytotoxin activity was detected on the murine L929 target cell in a 16-hr cytotoxicity assay. In contrast, several nonlytic T cell tumor lines failed to produce a soluble cytotoxin. Antibodies capable of neutralizing human alpha-lymphotoxin were completely ineffective in inhibiting the cytotoxin(s) produced by any of the cytotoxic T lymphocytes (CTL) cell lines. Comparative gel filtration and HPLC hydrophobic chromatography of alpha-lymphotoxin and CTL toxin produced by the CTL-830.B2 clone revealed significant differences in their elution profiles. The CTL-produced toxin and alpha-lymphotoxin exhibited similar kinetics of lysis of the L929 target cells, with 50% target cell lysis occurring at 10 hr. These data indicate human CTL produce a cytotoxin(s) antigenically distinct from alpha-lymphotoxin and imply that human cytolytic effector T cells are not the cellular source for the production of human alpha-lymphotoxin. The relationship of alpha-lymphotoxin and CTL toxin production was investigated in unseparated peripheral blood mononuclear cells stimulated with lectins or IL 2 for 1 and 5 days. Anti-alpha-lymphotoxin antibodies were capable of neutralizing only 30 to 50% of the cytotoxic activity in 24-hr supernatants. Cytotoxic activity in supernatants harvested after 120 hr stimulation with PHA or Con A was neutralized 70 to 100%, whereas the toxin(s) released from IL 2-stimulated lymphocytes was only neutralized 30%. These data suggest the observed heterogeneity of cytotoxic lymphokines produced by unseparated mononuclear cells depends in part on the subpopulations of effector cells responding to a given stimulus and the capacity of different subpopulations to produce distinct cytotoxins.

Modulation of natural killing by tumor promoters: the regulatory influence of adherent cells varies with the type of target cell

We have analyzed the regulatory effects of two classes of tumor promoters, phorbol diestersand indole alkaloids, on human natural killer (NK) cell activity {itin vitro}. In accordance with previous reports, we found that 12-O-tetradecanoylphorbol-13-acetate (TPA) inhibited natural killing against K 562 targets by unseparated mononuclear cells. Here, suppression of NK required the presence of adherent cells (macrophages). Contrary to the results obtained with K 562, tumor promoter-induced suppression of NK activity tested against U 937, another cell line of known NK susceptibility, was independent of the presence of adherent cells. Thus, NK cytotoxicity of effector cells rigorously depleted of adherent and Ia-positive cells was still inhibited when assayed against U 937, while it was generally enhanced when tested against K 562. Identical results were obtained with teleocidin and dihydroteleocidin B, two members of the recently discovered indole alkaloid class of tumor promoters. Therefore, we demonstrate that the regulatory effect of tumor promoters on human NK activity (suppression or stimulation) is determined not only by macrophages at the effector cell level but also by the type of target cell under study.

Increased IgG secretion by unstimulated mononuclear cells in active multiple sclerosis and functional assessment of the T8 subset

Unseparated mononuclear cells (10 5 cells/well) were cultured both in the presence and absence of pokeweed mitogen (PWM), and IgG secretion was measured by radioimmunoassay. In unstimulated cultures, levels of IgG secretion were found to be higher in a group of patients with multiple sclerosis (MS) than in control groups of healthy individuals or patients with other neurologic diseases (OND). By contrast, PWM-induced IgG secretion was similar in MS patients and in controls. In MS patients, levels of IgG secretion >2500 ng/ml in unstimulated cultures were present in 29 (58%) of 50 patients with active disease and in only 3 (14%) of 21 patients with inactive MS ( P < 0.01; MS active vs inactive). Furthermore, levels of IgG secretion in unstimulated cultures were higher in patients who had abnormalities of circulating T-cell subsets consisting of reduced numbers of suppressor/cytotoxic (T8) cells and elevated helper: suppressor (T4:T8) ratios. In additional experiments using isolated populations of T-cell subsets, T8 cells from MS patients who had low percentages of circulating T8 cells were found to suppress PWM-induced IgG secretion by autologous cells to a similar extent as controls, suggesting that in vitro, T8 cells function normally in these patients. In vitro IgG secretion by unstimulated mononuclear cells in MS appears to be a further reflection of abnormal immune regulation in this disease.

Natural killer cell activity in patients undergoing upper abdominal surgery: relationship to the endocrine stress response.

Natural killer (NK) cell activity and the endocrine response during and after parietal cell vagotomy were studied in two groups of patients receiving either epidural analgesia extending from S5 to Th4 + general anaesthesia (Group I), or general anaesthesia (Group II). NK cell activity of unseparated mononuclear cells in peripheral blood was measured against K-562 target cells in a 51Cr-release assay. NK cell activity increased in the same way in both groups in relation to premedication, anaesthesia and surgery (P less than 0.01). Postoperatively, the activity fell significantly on the first day (P less than 0.01), but returned to preoperative levels on day 3 (Group I) and day 5 (Group II). The endocrine response measured, except for adrenaline and prolactin, differed between Group I and II. In Group I, plasma noradrenaline and serum cortisol increased insignificantly throughout the observed period--compared to the preoperative level--whereas a significant increase in both hormones was found in Group II during surgery and in the postoperative period. A significant increase in plasma adrenaline and serum prolactin was found in both groups during anaesthesia and surgery. The findings indicate that NK cell activity during upper abdominal surgery is modified in almost the same way during two different anaesthetic techniques, one of which partly seemed to block the endocrine surgical stress response. The fluctuations in NK cell activity were not correlated to the changes measured in hormone concentrations.

Regulation of natural killer cell activity by macrophages in the rheumatoid joint and peripheral blood.

Recently, in another study, we observed that indomethacin, a prostaglandin synthetase inhibitor, significantly increased NK activity in both normal and rheumatoid arthritis (RA) peripheral blood (PB) but not in RA synovial fluid (SF). Because macrophages are a major source of prostaglandins, we examined the effect of macrophage-enriched adherent cells (AC) on NK activity as measured by a 3-hr Cr-release assay with K 562 cells. The removal of AC resulted in increased (p less than 0.01) NK activity in both normal and RA PB. In contrast, the removal of AC from RA SF resulted in a significant decrease (p less than 0.001) of NK activity. By using only nonadherent cells (NAC), NK activity in RA SF and synovial tissue (ST) was significantly reduced when compared to autologous RA PB (p less than 0.001). Enhancement of NK activity of SF NAC by both poly I:C and IL 2 was not dependent on AC. Mixing experiments demonstrated that the addition of synovial AC for 16 hr increased NK activity of synovial NAC to a level similar to that of unseparated mononuclear cells, whereas autologous PB AC suppressed NK activity of PB NAC. PB AC, when added to SF NAC, also increased NK activity. Supernatants from synovial mononuclear cells were stimulatory of synovial NAC NK activity, whereas normal PB mononuclear supernatants were suppressive. These observations document 1) a significant reduction of NAC-mediated NK activity in the rheumatoid joint as compared to PB from the same patient, and 2) that AC modulate NK activity differently in the rheumatoid joint as compared to RA or normal PB.

Capacity of human large granular lymphocytes (LGL) to produce multiple lymphokines: interleukin 2, interferon, and colony stimulating factor.

Human large granular lymphocytes (LGL), which are known to be responsible for natural killer (NK) cell activity, also produced a variety of lymphokines including interleukin 2 (IL 2), colony stimulating factor (CSF), and interferon (IFN) in response to phytohemagglutinin (PHA) or concanavalin A (Con A). Human peripheral blood LGL, which were purified by removal of monocytes adhering to plastic flasks and nylon columns, followed by separation on a discontinuous Percoll gradient, and additional treatment with anti-OKT3 and Leu-M1 plus complement, were more potent producers of these lymphokines than unseparated mononuclear cells (MNC), nylon column-eluted cells, or purified T lymphocytes. Moreover, IL 2 production by LGL could be further distinguished in that it was not enhanced by the addition of macrophages or macrophage-derived factor, i.e., IL 1, whereas addition of macrophages did potentiate IL 2 production by T lymphocytes. Further analysis of cells in the LGL population using various monoclonal antibodies revealed that removal of cells with OKT11 or AF-10, a monoclonal antibody against human HLA-DR antigen, decreased IL 2 production, whereas removal of OKT8+, OKM1+, Leu-M1+, or Leu-7+ cells led to enhanced IL 2 production. The LGL population is therefore heterogeneous and includes at least three functionally and phenotypically distinct subsets. An atypical T cell subset (OKT3-, Leu-1-, OKT11+) rather than the myeloid subset of LGL (Leu-M1+ or OKMI+) was the source of LGL-derived IL 2, whereas the latter subset and/or another subset of OKT8+ cells appear to regulate this IL 2 production. In addition to performing NK activity, LGL on a per cell basis seem to be more effective than T lymphocytes in producing lymphokines, namely, IL2, CSF, and IFN.

Establishment of spontaneously outgrowing lymphoblastoid cell lines with Cyclosporin A.

To establish spontaneously outgrowing EBV (Epstein-Barr virus) transformed lymphoid cell lines from healthy EBV-seropositive adults different culture conditions were investigated. The effect of T-cell depletion was compared with that of adding Cyclosporin A (CSA) to unseparated mononuclear blood cells, either at the onset of cultivation or after 3 weeks. The highest frequency of spontaneous outgrowth of EBV-transformed cells was obtained in unseparated cultures when the addition of CSA was delayed. The presence of unimpaired T cells at the onset of the culture period appeared to have a favourable effect on the spontaneous outgrowth of EBV-carrying lymphoblastoid cell lines.

Density separation of chronic lymphocytic leukemia cells: Low-density non-T cells are efficient stimulator cells in allogeneic and autologous mixed leukocyte reaction

Unseparated mononuclear cells and E rosette-depleted non-T cells from a majority of patients with chronic lymphocytic leukemia (CLL) were found to be weak stimulators in the allogeneic mixed-leukocyte reaction (MLR). However, a minor population (1–5%) of highly active stimulator cells could be isolated from all patients studied by buoyant density centrifugation using discontinuous gradients of Percoll. The same low-density non-T-cell fraction also stimulated autologous T-cell proliferation in the autologous mixed-leukocyte reaction (AMLR). In contrast, Percoll-separated high-density non-T cells, including the leukemic B-cell pool, were completely inactive as stimulators in AMLR. These results suggest that the presence of efficient stimulator cells among CLL mononuclear cells may be masked by the large number of nonstimulating leukemic B cells.

Determination of IgG subclasses and Gm allotypes in culture supernatants of pokeweed mitogen-stimulated human blood lymphocytes.

Concentrations of the 4 IgG subclasses, of IgM, and of IgA were determined in culture supernatants of pokeweed mitogen-stimulated mononuclear cells isolated from human peripheral blood. Time-course studies showed cumulative secretion of IgM, IgA, and the subclasses IgG1, IgG2, and IgG3 but not of IgG4. In supernatants of 7-day cultures of unseparated mononuclear cells, IgG1 was predominant, followed by IgG2 and IgG3. Removal of most monocytes from the mononuclear cells resulted in an overall decrease of immunoglobulin production but had no influence on the relative IgG subclass distribution. In supernatants of T cell-enriched cultures, the synthesized IgG was deficient in IgG1. Likewise, in supernatants of B cell-enriched cultures, IgG2 exceeded IgG1 concentration. Elimination of the T gamma cells suggested some influence of this subset on IgG2 production. Gm allotypes determined in supernatants corresponded to those in serum of the blood donors.

Regulation of antigen-induced lymphoproliferation by BSA gradient-separated T cell fractions.

Human T cells from 6 volunteers immunized with keyhole limpet hemocyanin (KLH) or tetanus toxoid were fractionated on bovine serum albumin (BSA) gradients. These T cell fractions were then recombined with autologous unseparated mononuclear cells or unseparated T cells to determine the effect of each fraction on the proliferative (DNA synthetic) response to the immunizing antigen. Using this separation technique, we were able to define 2 fractions of T cells of widely different densities that had a suppressive effect on the proliferative response to KLH of unfractionated T cells. The demonstration of suppressive activity was possible only if cells were tested within 8 wk of immunization with KLH. These suppressive T cell fractions differed not only in density but also in surface characteristics. Fraction 1 cells had a high proportion of Ia+ cells but no Fc receptors for IgG (FcRG-) were seen, whereas cells from fraction 4 (of higher density) were Ia- and were composed of 12.1 +/- 1.2% FcRG+ cells. this suppression was shown to be specific for the immunizing antigen. One individual who had been immunized with KLH for more than 1 yr in which suppression of KLH-induced proliferation was no longer demonstrable was given primary immunization to tetanus toxoid. Suppression could be demonstrated in fractions 1 and 4 specific for tetanus toxoid; there was no demonstrable effect of these T cell fractions on the response to KLH. We postulate that these are different functional populations of suppressor T cells that regulate antigen specific lymphoproliferation.

Antibody‐Dependent Monocyte‐Mediated Cytotoxicity

Among mononuclear cells isolated from human blood monocytes exclusively mediated antibody‐dependent cytolysis of human type B erythrocytes. Adherent monocytes detached from plastic surfaces by lowering the temperature to 4°C expressed the same cytotoxicity as monocytes contained in the unseparated mononuclear cell fractions. No difference was observed in the cytotoxicity of non‐adherent monocytes and of monocytes remaining adherent at 4°C and subsequently mechanically removed. Removal of carbonyl‐iron phagocytosing monocytes reduced the number of latex‐phagocytosing monocytes without influencing cytotoxicity of the remaining monocytes. In vitro cultivation for 24h of unseparated mononuclear cells and of purified monocyte suspensions increased the number of latex‐positive cells, leaving the number of esterase‐positive cells and the cytotoxicity unchanged.

Human intestinal mononuclear cells: I. Investigation of antibody-dependent, lectin-induced, and spontaneous cell-mediated cytotoxic capabilities

Cytotoxic mononuclear cells may mediate inflammatory bowel disease but have not been demonstrated in human intestinal mucosa. Therefore, we have examined human intestinal specimens for the presence of cytotoxic mononuclear cells and lymphocytes. Using a sequential dithiothreitol-EDTAcollagenase technique, we examined mononuclear cells obtained from mucosa of 37 intestinal specimens consisting of inflammatory bowel disease or normal control tissue adjacent to tumor or diverticular disease, all obtained at surgery. Surface characteristics revealed a mean of 7% ± 1% Fc receptor bearing cells for control colon and 6% ± 2% for inflammatory bowel disease intestine. Lectin-induced cellular cytotoxicity with human red blood cells as targets was seen with unseparated mononuclear cells and macrophage depleted lymphocytes from peripheral blood (64% and 46%, respectively), control colons (22%, 19%) ulcerative colitis colons (29%, 18%), and Crohn's intestinal specimens (43%, 29%). Antibody-dependent cellular cytotoxicity with chicken red blood cells as targets was also seen with unsepa rated mononuclear cells and macrophage-depleted lymphocytes from peripheral blood (44% and 45%, respectively) control colons (15%, 24%), ulcerative colitis colons (24%, 20%), and Crohn's intestinal specimens (17%, 13%). In contrast, using Chang cell lines as targets, antibody-dependent cellular cytotoxicity was observed with peripheral blood mononuclear cells but not with control or inflammatory bowel disease intestinal cells. Spontaneous cell-mediated cytotoxicity against Chang or K562 cell lines was also not observed with intestinal cells. These experiments demonstrate that Fc-receptor bearing mononuclear cells are present in control and IBD human intestinal mucosa. Furthermore, lamina propria lymphocytes from control and inflammatory bowel disease intestine mediate lectin-induced cellular cytotoxicity against human red blood cells and antibody-dependent cellular cytotoxicity against chicken red blood cells, but do not mediate cytotoxicity against cell line cells.