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PubMed2000

Inhibition of platelet function by GSTM1-null human peripheral lymphocytes exposed to benzo(a)pyrene-induced challenge.

Recent epidemiological studies proposed that the glutathione S-transferase (GST) M1-null genotype may contribute to diseases associated with oxidative stress. The genetic polymorphism exhibited by the GSTM1 may be an important factor in risk toward oxidant chemicals. In this study, we investigated the effect of GSTM1-null genotype in lymphocyte and oxidative stress-dependent inhibition of platelet aggregation. To determine whether GSTM1 deficiency is a genetic determinant of cell toxicity toward oxidant chemicals, lymphocytes were incubated in vitro with low levels of benzo(a)pyrene (BaP), cumene hydroperoxide (CumOOH), or trans-stilbene oxide that do not decrease cell viability, and were assessed for oxidative damage and for the lymphocyte-dependent inhibition of platelet response. Malondialdehyde and carbonyl levels, and the oxidation of cisparinaric acid, were used as biomarkers of oxidative stress in lymphocytes. Following stimulation by BaP or CumOOH, when peroxidation-dependent changes in these parameters were compared between the GSTM1-null genotype and the positive genotype, no significant differences were found between the two genotypes. On the other hand, preincubation of the lymphocytes with BaP or CumOOH attenuated their inhibitory action on ADP-induced platelet aggregation. However, our results indicate that lymphocytes of individuals with the GSTM1-null genotype have greater inhibitory activity on platelet function after exposure to BaP, but not CumOOH, although they are not more susceptible to in vitro oxidative stress.

Adult↗
PubMed1995

[Hodgkin disease: recent histological and biological data].

Recent histologic, immunophenotypic and genotypic data have restricted the concept of Hodgkin's disease (HD) to the type 2 and 3 of Rye classification. This classification should be revised since the lymphocyte-predominance type has been shown to include the nodular paragranuloma which is a B-cell lymphoma, cases which have been confused with T-cell-rich large B-cell non Hodgkin's lymphoma (NHL) and cases which should be reclassified among the mixed cellularity group. Further more, most types 4 are now regarded as anaplastic large cell NHL. Immunophenotypic and genotypic studies support the heterogeneous nature of Reed-Sternberg and Hodgkin's (RSH) cells since they could be derived from B, T or null lymphocytes. In 50% of cases, RSH cells harbour the Epstein-Barr virus genome and express a viral protein, the latent membrane protein, which could play an oncogenic role in HD. Finally, RSH cells produce a wide range of cytokines that could stimulate their proliferation and explain the marked cellular reaction that is observed in HD.

Cytokines↗
PubMed1977

Phytohemagglutinin-induced differentiation and blastogenesis of precursor T cells from mouse bone marrow.

The cells in mouse bone marrow (BM) capable of responding to phytohemagglutinin (PHA) were shown to be precursor T cells in experiments employing athymic mice, immunofluorescence, and specific lysis of T or B cells with cytotoxic antisera + complement. In contrast, the responses of lymph node (LN) and spleen (Spl) cells to this mitogen were shown by the same techniques to rely upon resident populations of mature T lymphocytes in these peripheral lymphoid organs. Cytolysis of T cells with anti-theta (anti-Thy 1), anti-thymocyte, or anti-brain antisera abolished the PHA responses of LN and Spl, but had no appreciable effect on the BM PHA response. Lysis of B cells with anti-mouse gamma globulin or anti-mouse IgM antisera had no significant effect on either Spl or BM blastogenesis in response to this lectin. Immunofluorescent studies with fluoresceinated anti-brain sera demonstrated acquisition of T-cell surface antigens by BM null lymphocytes during the blastogenic response of this tissue to PHA. The results of these immunofluorescence experiments were reproducible even when marrow obtained from nude mice and pretreated with anti-brain serum plus complement was employed. The implications of these findings with regard to prophylaxis against graft versus host disease in BM transplant recipients are discussed.

Animals↗
PubMed1984

Defective expression of T cell antigens in chronic lymphocytic leukaemia: relationship to T cell dysfunction.

In chronic lymphocytic leukaemia (CLL) peripheral blood T cells have a variety of functional abnormalities. To explore more extensively the T cell status of B-CLL patients, surface immunoglobulin-negative cells were isolated by sheep erythrocyte rosetting (ER) and the membrane phenotypes of the ER + cells defined by immunofluorescence utilizing monoclonal antibodies (MAb). In 11 of 18 CLL patients (CLL group I) there was excellent correlation between ER + and T3 (mature T cell marker) positivity. In the remaining patients (CLL group II), only 5-45% of ER + cells were T3 positive, suggesting that many rosetting cells were non-T. However, the ER +, T3 negative cells were nonreactive with OKM -1 (MAb which detects monocytes and 'null' lymphocytes) or with OKT11, 9.6, and 35.1, MAb against the T cell E receptor. Moreover ER +, T3 negative cells were not stained with OKT4, OKT8, OKT6, OKT9 , or OKT10 . Treatment of group II ER + cells with neuraminidase increased (from 27% to 74%) the mean percentages of T3 positive cells detected, but not other membrane antigens. ER + cells from group II patients, compared with normal and group I patients, exhibited diminished proliferative responses to PHA and Con-A (P less than 0.01) and supported poorly pokeweed mitogen-induced proliferation of normal allogeneic B cells (P less than 0.01). Thus, in approximately one-third of the CLL patients studied, many ER + cells poorly express a number of membrane antigens characteristic of normal mature T cells, one of which (T3) is unmasked by neuraminidase treatment. This phenotypic abnormality appears to be associated with significant T cell dysfunction in vitro and may, at least in part, contribute to the commonly encountered immunological defects present in these patients.

Antibodies, Monoclonal↗
PubMed2004

CD4+CD28- T lymphocytes contribute to early atherosclerotic damage in rheumatoid arthritis patients.

BACKGROUND: Peripheral blood expansion of an unusual CD4+ T-cell subset lacking surface CD28 has been suggested to predispose rheumatoid arthritis (RA) patients to develop more aggressive disease. However, the potential association between CD4+CD28null T cells and early atherosclerotic changes in RA has never been investigated. METHODS AND RESULTS: The number of circulating CD4+CD28null cells was evaluated in 87 RA and 33 control subjects who also underwent evaluation of carotid artery intima-media thickness (IMT) and endothelial function via flow-mediated vasodilation (FMV). Patients had higher IMT and lower FMV compared with control subjects. The frequency of CD4+CD28null cells was significantly higher in patients than in control subjects. Twenty patients with persistent expansion of circulating CD4+CD28null cells had more marked increase of carotid artery IMT and stronger decrease of brachial artery FMV. Blockade of tumor necrosis factor-alpha led to a partial reappearance of the CD28 molecule on the CD4+ cell surface. CONCLUSIONS: Circulating CD4+CD28(null) lymphocytes are increased in RA. Patients with persistent CD4+CD28null cell expansion show preclinical atherosclerotic changes, including arterial endothelial dysfunction and carotid artery wall thickening, more significantly than patients without expansion. These findings suggest a contribution of this cell subset in atheroma development in RA. Moreover, the demonstration that tumor necrosis factor-alpha blockade is able to reverse, at least in part, the CD28 deficiency on the CD4+ cell surface may be of interest for possible innovative therapeutic strategies in cardiovascular diseases.

Aged↗
PubMed1986

Murine lymphokine-activated killer (LAK) cells: phenotypic characterization of the precursor and effector cells.

Murine and human lymphocytes incubated in recombinant interleukin 2 (RIL 2) generate a population of cytotoxic cells (lymphokine-activated killer cells [LAK]), which are able to lyse a wide array of fresh tumor cells but do not lyse fresh normal cells. Intravenous administration of these cells with the concomitant administration of RIL 2 can eliminate established pulmonary and hepatic metastases in mice. To characterize the cell that has in vitro LAK activity, we subdivided murine lymphocytes by lysing select subpopulations with the use of complement and antibodies against lymphocyte surface markers or by fluorescence-activated cell sorting. Thy-1.2-negative splenocytes were found to generate near normal amounts of LAK activity after RIL 2 incubation. Small and inconsistent LAK cell activity was generated from Thy-1.2-positive splenocytes. Ia-positive and surface immunoglobulin-positive splenocytes had little or no LAK precursor capability and did not appear to be necessary for LAK activation. Treatment of splenocytes with anti-asialo GM1 (anti-ASGM1) heterosera and complement markedly decreased their ability to generate LAK activity. At the effector stage, cytotoxic cells were of the Thy-1.2-positive, Ia-negative phenotype. Ia-depleted cells were separated into subpopulations bearing or not bearing the gamma Fc receptor (gamma FcR). The majority of cytotoxicity resided in gamma FcR-positive cells. Thus the precursors of murine LAK cells are "null" lymphocytes bearing neither T nor B cell surface markers but develop the Thy-1.2 cell surface marker in vitro, in association with the development of lytic activity for fresh tumor cells after stimulation by RIL 2.

Animals↗
PubMed1981

Immunodepression in trypanosome-infected mice. VI. Comparison of immune responses of different lymphoid organs.

Mitogen stimulation of cells from various lymphoid organs of C3H/He mice chronically infected with an isolate of Trypanosoma congolense was studied at different time intervals after infection, using concanavalin A (Con A) and lipopolysaccharide (LPS). At the same time, changes in the percentages of T, B and null lymphocytes in these organs were determined by immunofluorescence staining. The responses of T and B lymphocytes in the spleen were totally depressed, and the cellular composition was drastically altered by day 14 after infection. Unlike the spleen, the lymph nodes showed minor changes in their T and B lymphocyte responses and cell composition during the course of the infection, except the B cell response and composition which were altered late in the infection. The thymus and bone marrow did not show any appreciable changes in their mitogen responses and cell composition throughout the infection. The peripheral blood lymphocytes showed reduced B cell responses. Spleen cells from chronically infected mice suppressed lymphocyte stimulation induced in normal spleen and lymph node cell populations by Con A, LPS and allogeneic stimulator cells. Lymph node cells from the same group of mice did not exhibit any such suppressor activity. In the experimental system used here, the spleen is the primary site of immune depression, and other lymphoid organs such as the lymph nodes and thymus are very little affected.

Animals↗
PubMed1997

Morbidity in a large cohort study of children born to mothers exposed to radiation from Chernobyl.

Reproductive health was reviewed in four oblasts of the Republic of Belarus that were either heavily exposed (Mogilev and Gomel) or lightly exposed (Brest and Vitebsk) to ionizing radiation after the meltdown of a nuclear reactor in Chernobyl. A retrospective analysis was conducted on pregnancies occurring between January 1, 1982, and December 31, 1990, and a comparison of results was made between pregnancy outcomes prior to and after the meltdown for individuals residing in heavily exposed and lightly exposed oblasts. Pregnant women who resided in heavily exposed oblasts appeared to be at risk for development of toxemia, renal insufficiency and anemia. Neonates born in heavily contaminated areas were apparently at risk for development of anemia and congenital malformations and perinatal death. In addition, a cohort of 757 neonates, 0-18 months old, with a normal physical examination, was identified for laboratory analysis of hematological, immunological, endocrinological and nutritional status. Decreased levels of copper and zinc were documented in erythrocytes from neonates from heavily contaminated oblasts, findings that may be related more to inadequate nutrition than to radiation exposure. Increased absolute "null" lymphocyte number and diminished absolute T lymphocyte number with a reduction in the "helper" (i.e., T4) subclass of T cells were evident in neonates born-in heavily exposed oblasts. Geographic differences in reproductive health and immune status are apparent in Belarus that may be related to radiation exposure. Additional studies are required to exclude confounding variables and possible selection bias.

Abnormalities, Radiation-Induced↗
PubMed1979

Primary malignant lymphoma of the CNS and polyneuropathy in a patient with necrotizing vasculitis treated with immunosuppression.

A woman, aged 58, who had undergone prolonged treatment with corticosteroids for generalized necrotizing vasculitis, and had received azathioprine (Imurel) for 18 months, 4 years after discontinuing the latter treatment, developed peripheral neuropathy and a rapidly progressing cerebral disorder suggesting a basal meningeal process. CSF cytology suggested malignant lymphoma with meningeal involvement. Immunological studies showed an increase of Null-lymphocytes in the peripheral blood. Autopsy disclosed a primary malignant lymphoma of the CNS with the histological appearance of a multilocular immunoblastoma showing almost ubiquitous meningocerebral involvement. Clinical and postmortem examinations failed to demonstrate any systemic extraneural lymphoproliferative disorder. In addition, there was peripheral polyneuropathy of the axonal type with denervation atrophy of skeletal muscle, but without lymphomatous involvement of the neuromuscular system. The possible relations between primary malignant lymphomas of the CNS and previous immunosuppressive treatment of immunoinflammatory disease are discussed in view of the concept of impaired immunoregulation. The pathogenetic background of peripheral polyneuropathy is unknown.

Azathioprine↗
PubMed1989

Characterization of bovine mononuclear cell populations with natural cytolytic activity against bovine herpesvirus 1-infected cells.

Freshly isolated or overnight cultured peripheral blood mononuclear cells from immune or nonimmune animals had natural cytolytic activity against bovine herpesvirus 1 (BHV-1)-infected tumor target cells. No lysis was demonstrated against tumor target cells alone. This natural cytolytic activity was present in mononuclear cells from the spleen, lymph node, and peripheral blood but little or no cytolytic activity was detected in bone marrow or thymus cells. When monoclonal antibodies and complement to deplete bovine mononuclear cell subpopulations from the nonadherent cells were used, results indicated the effector cell was not a T cell, B cell, or activated monocyte. From nonadherent populations separated on density gradients, it was determined that the effector cells were large, low density mononuclear cells. These results indicate the nonadherent effector cells mediating lysis of BHV-1-infected xenogeneic adherent target cells were large null lymphocytes and/or immature monocytes.

Animals↗
PubMed1980

Immunological indices in presenile Alzheimer's disease.

Immunological indices, both T- and B-dependent, were studied in 11 patients affected by presenile Alzheimer's disease. The data obtained were compared with those from a group of normal adults of similar age and from a group of normal young subjects. Furthermore, antisera were produced in rabbits against Alzheimer's serum and compared to antisera against normal human serum. The following results were obtained: decrease of serum IgM levels; no monoclonal aspects or auto-antibodies were detected in our patients. The kappa/lambda ratio was also normal. The T cell system was functionally normaly, but with a slight decrease of the T cell number and with an increase of the Null lymphocytes. No specific serum proteins were found in the anti-Alzheimer antisera. The data are discussed in correlation to the possible genesis of senile plaques.

Alzheimer Disease↗
PubMed1994

The Null/gamma delta TCR+ T cell family in the pig.

The very large population of highly thymus-dependent, non-adherent 'Null' blood lymphocytes in young pigs, which lack most surface markers characteristic of classical T-cell subsets, have recently been shown to bear several novel population- and subset-specific antigens and gamma delta T-cell receptors. These T-lymphocytes differ radically from conventional CD2-positive T-cells in their origins, biological lifespan, tissue distribution, migration behaviour, cell surface phenotype, immunological responsiveness and mechanisms of trafficking through constitutive lymphoid tissues and inflammatory lesions. Elucidation of the roles of these enigmatic cells and their characteristic surface macromolecules in the initiation and regulation of immune functions promises to reveal much of fascination.

Animals↗
PubMed1992

Kinetics of immune cell and bone resorptive responses to endodontic infections.

Infection of the dental pulp stimulates a host immune response in the periapical region (the periapical "lesion") with the concomitant resorption of bone. The cell composition of human or rat periapical lesions is mixed, consisting of T, B, and "null" lymphocytes, plasma cells, macrophages, polymorphonuclear leukocytes, and mast cells. Cells are thus present which mediate a broad spectrum of immunological phenomena. In order to determine which of these mechanisms contribute to periapical bone resorption, a rat model system has been used in which periapical lesions are induced by pulp exposure and infection from the oral environment. In this model, a rapid period of lesion expansion and bone destruction occurs between days 1 and 15 after exposure (active phase), with a chronic phase characterized by lesion stabilization commencing thereafter. Phenotypic analysis of the cellular infiltrate has shown that T helper cells predominate during the active phase, whereas increased numbers of T suppressor cells are associated with chronicity. Extracts of periapical lesions contain bone-resorbing activity, as determined by the release of 45Ca from prelabeled a rat long bones in organ culture. Higher levels of bone-resorbing activity are present during the active than in the chronic phase. Characterization of bone-resorbing activity indicates the presence of resorptive mediators which are heat labile and protease sensitive and which are distinct from lipopolysaccharide. Preliminary biochemical fractionation indicates that resorptive mediators fractionate in the 15,000- to 60,000-dalton molecular mass range, presumably cytokines such as interleukin 1 and tumor necrosis factor. These studies demonstrate the utility of the rat model for studying mechanisms of periapical lesion pathogenesis and implicate T helper cell-mediated activities, in particular those leading to macrophage activation and cytokine production, in periapical lesion expansion.

Alveolar Bone Loss↗
PubMed1977

Circulating thymic-hormone activity in congenital immunodeficiency.

Circulating thymic-hormone activity was assayed by measuring Thy 1-2 antigen induction on null lymphocytes from athymic mice incubated with human plasma or serum. Plasma from 19 normal children aged under 10 had inductive activity equivalent to 10-6-16-2 ng thymopoitin/ml. Plasma from 15 infants were severe combined immuno-deficiency, 2 of whom had appreciable immunoglobulin synthesis, and from 2 infants with DiGeorge syndrome had little or no inductive activity. Successful reconstitution with thymus or bone-marrow grafts and with red-cell infusions (if adenosine-deaminase deficiency is present) was followed by a rise in circulating thymic-hormone activity.

Agammaglobulinemia↗
PubMed1977

Bioassay determinations of thymopoietin and thymic hormone levels in human plasma.

Thymopoietin is a thymic hormone that induces differentiation of thymocytes from precursor cells which arise in hemopoietic tissues. This paper describes a sensitive in vitro assay for the induction of Thy 1.2 antigen on null lymphocytes from germ-free athymic (nu/nu) mice. The sensitivity and specificity of the bioassay were increased by adding high concentrations of ubiquitin (a nonspecific inducer) to the induction incubations. The bioassay was sufficiently sensitive to detect thymopoietin at less than 0.25 ng/ml. A dose-response relationship was shown between thymopoietin concentration and the percentage of cells induced to express Thy 1.2 antigen. When normal human plasma was assayed, induction was registered with activity corresponding to thymopoietin at greater than 1 ng/ml in plasma from infants or young adults. Activities in the thymopoietin range of 0.25 ng/ml were registered with plasma from healthy subjects over 50 years of age. Thymectomy was followed by loss of this inductive activity from the plasma. This bioassay permits clinical studies on T (thymus-derived) cell inducers released by the human thymus into the circulation.

Adult↗
PubMed1980

Purificaton of a functional mouse Fc receptor through the use of a monoclonal antibody.

We recently reported the isolation of a rat monoclonal antibody designated 2.4G2 (9) that is directed against the mouse trypsin-resistant Fc receptor (FcR) for IgG2b and IgG1 immune aggregates. We have now utilized the Fab fragment of 2.4G2 as an affinity reagent to purify FcR from the macrophage cell line J774 to apparent homogeneity. The antigen isolated from J774 cells consisted of two general types of polypeptides with broad electrophoretic mobilities of approximately 60,000 and 47,000 mol wt. Similar broad bands ranging from 47,000 to 70,000 mol wt were isolated from various FcR-bearing cell lines of B, T, and null lymphocyte, as well as of macrophage origin. J774 FcR was judged to be a glycoprotein based on the sensitivity of its isoelectric point to neuraminidase digestion, its labeling with galactose oxidase/NaB[3H4], and its binding to concanavalin A-Sepharose. In phosphate-buffered saline, the isolated protein formed large aggregates that were shown to retain FcR activity, albeit with a somewhat altered IgG subclass specificity. The FcR aglutinated erythrocytes that were coated with both IgG2b and IgG2a that did not otherwise hemagglutinate. In addition, iodinated FcR bound to Sephadex beads coated with rabbit IgG, mouse IgG1, IgG2b, and IgG2a, but not to beads coated with mouse IgG3 or rabbit F(ab')2 fragments. The binding of the purified receptor to all IgG classes was inhibited by the Fab fragments of 2.4G2. In contrast, the binding of IgG2a to intact macrophages was inhibited by 2.4G2 Fab by only 15%, whereas rabbit IgG immune aggregate binding was almost completely abolished.

Animals↗
PubMed1987

Rearrangement and expression of T cell receptor genes in cloned murine natural suppressor cell lines.

Naturally occurring suppressor cells of the in vitro mixed leukocyte culture reaction and of in vivo graft-vs.-host disease have been identified in the spleens of neonatal mice (1) and of adult mice recovering from total lymphoid irradiation (2), whole-body irradiation (3), and syngeneic marrow transplantation (4), or cyclophosphamide therapy (5). Using both positive and negative selection procedures, the suppressors were reported to be null lymphocytes that did not express mature macrophage surface markers, nor differentiate into mature macrophages in vitro, nor demonstrate natural killer (NK) activity (1). Subsequently, cloned lines of these natural suppressor (NS) cells were derived from either adult mice given total lymphoid irradiation (TLI) (2) or from neonates (6). The cloned NS cell lines expressed a surface phenotype (2, 6) similar to that reported previously for cloned NK cells (Thy-1(+), asialo-GM1(+), Ig(-), Lyt-1(-), Lyt-2(-), Ia(-), MAC-1(-)) (7-9). However, the NS cells did not show NK activity in the standard assay with YAC-1 target cells. The cloned NS lines suppressed the proliferation of responder cells and the generation of cytolytic cells in the mixed leukocyte reaction (MLR), and suppressed lethal graft-vs.-host disease in vivo (10, 11). In view of the unusual function and surface phenotype of the cells, the lineage of these cells remained unclear. To determine the lineage of the cloned NS cells, we searched for expression and rearrangement of the alpha and beta chain genes of the T cell antigen receptor, as well as that of the gamma chain gene. Studies of the phenotypically similar NK cell yielded conflicting results. Thus, cloned lines of murine NK cells were reported to have rearrangements of the beta chain genes, and to express mRNA for all three chains (12). In contrast, freshly purified rat or human large granular lymphocytes (LGL) were shown to express only the 1.0 kb mRNA species of the beta chain gene (13), indicative of D-J joining (14). Thus, some but not all cells with NK function express the T cell receptor and are members of the T cell lineage. The current report shows that the NS lines express full-length mRNA transcripts for the a and beta chain of the T cell receptor, as well as the gamma chain gene.

Animals↗