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Biomedical subjects

I Green

Publications and source records attributed to I Green.

At least 73 records · Page 4Linked to original sources
PubMed1982

Defective regulation of B lymphocyte colony formation in patients with systemic lupus erythematosus.

We have succeeded in generating B cell colonies from freshly separated human peripheral blood by the double agar layer technique and expanding them in liquid culture for several weeks. Populations of cells enriched in B cells were placed into the upper layer with or without bacterial LPS. Although B cell colonies were observed without LPS, the addition of LPS to the cells in the upper agar layer increased the number of colonies. Also necessary for optimal B cell colony formation was the presence in the lower agar layer of either culture supernatant of PHA-stimulated mononuclear cells or purified T cells and PHA. Without such helper factors in the lower layer, only a few B cell colonies were observed in the upper layer. By using these techniques, peripheral blood lymphocytes from normal individuals and patients with active systemic lupus erythematosus (SLE) were studied for the generation of B cell colonies. Significantly more B cell colonies were observed in patients with SLE, using either kind of "helper" factor. In addition, T cells from normal individuals and patients were tested for their ability to help B cell colony formation. The SLE T cells were found to be defective in this function relative to normal T cells. Thus, although patients with SLE were hyperactive in forming B cell colonies, thier T cells were defective in supporting the formation of B cell colonies from normal individuals.

B-Lymphocytes↗
PubMed1981

Long-term culture and cloning of nontransformed human B lymphocytes.

B lymphocyte-enriched cell populations cultured with mitogens in initial suspension cultures formed colonies in soft agar when the same mitogenic agent was present in the lower layer of a two-layer soft agar system. Colony formation depended upon the presence of T cells in the initial culture, and was optimal after an initial 72-h culture with phytohemagglutinin (PHA; 12.5 microliters/ml), pokeweed mitogen (PWM; 2.5 micrograms/ml), or protein A (10 micrograms/ml). The colonies could be picked from the agar and propagated by feeding every 3 d with medium supplemented with a growth factor-containing tissue culture supernate. The growth factor-containing supernate was prepared by stimulating pools of human peripheral blood mononuclear cells for 72 h with PHA or PWM. The lines propagated in this manner were membrane Ig+, lacked sheep erythrocyte rosette-forming ability, and did not ingest latex. They lacked the Epstein-Barr nuclear antigen (EBNA) and had 46 chromosomes. Such lines have been propagated for over 1 yr. One line (BL1) was subjected to limiting dilution cloning and a line, BL1.1, was prepared that contained 96% lambda-bearing cells and no kappa-bearing cells. This line was also EBNA negative. This procedure can thus be used to prepare and clone long-term lines of nontransformed human B lymphocytes.

B-Lymphocytes↗
PubMed1981

Murine syngeneic mixed lymphocyte response. I. Target antigens are self Ia molecules.

A system has been described that produces a murine syngeneic mixed lymphocyte response (MLR) comparable in magnitude to an allogeneic MLR. The responder cells in these cultures exhibit the classic immunologic characteristics of both memory and specificity. Studies using radiation-induced bone marrow chimeras of F(1) {arrow} parent type indicated that, similar to many other T cell-mediated immune responses, the response of the T lymphocytes in the syngeneic MLR was major histocompatibility complex-restricted and was determined by the environment in which the T cells matured. Using responder T cells from F(1) {arrow} parent chimeras and stimulator cells from H-2 recombinant strains, it was possible to map the genes involved in the stimulation to the K and/or I regions. In addition, blocking studies with monoclonal anti-Ia antibodies suggested that in the B10.A strain the critical molecules were products of both the I-A(k) and I-E(k) subregions. The issue of whether the syngeneic MLR is directed solely at self I-region antigens or whether the response represents proliferation to an unknown antigen in association with self I-region determinants was also addressed. Secondary syngeneic MLR were successfully performed in normal mouse serum and with stimulator cells prepared in the absence of bovine serum albumin to rule out the possibility that xenogeneic serum antigens were involved in the stimulation. The possibility that the syngeneic MLR might represent a secondary response to environmental antigens was eliminated by using germ- free mice as a source of stimulator cells and by demonstrating that spleen cells from unimmunized, fully allogeneic chimeras (B10.A {arrow} B10) could generate a normal syngeneic MLR even though such chimeras could not be primed to respond to any foreign antigens unless supplemented in vivo with a source of antigen-presenting cells syngeneic to the B10 host. The possibility that the syngeneic MLR was a primary response to a foreign antigen was considered unlikely because by using our culture conditions we could not obtain a primary antigen response or a secondary antigen response after in vitro priming to a variety of potent foreign antigens. Finally, the possibility that the syngeneic MLR represents a response to a variety of minor histocompatibility self antigens in association with self Ia molecules was eliminated by showing that the secondary responses to H-2 compatible, non-H-2 different strain (A/J vs. B10.A and C3H, or BALB/c vs. B10.D2 and DBA/2) were comparable to the secondary responses to syngeneic stimulators. Thus, we conclude that the target antigens in the syngeneic MLR are solely determinants on self Ia molecules, although the functionally equivalent possibility of a single, nonpolymorphic, minor self antigen seen in association with self Ia molecules cannot be excluded.

Animals↗
PubMed1981

Falciparum malaria-infected erythrocytes specifically bind to cultured human endothelial cells.

Erythrocytes infected with the late stages of the human malarial parasite Plasmodium falciparum became attached to a subpopulation of cultured human endothelial cells by knoblike protrusions on the surface of the infected erythrocytes. Infected erythrocytes did not bind to cultured fibroblasts; uninfected erythrocytes did not bind to either endothelial cells or fibroblasts. The results suggest a specific receptor-ligand interaction between endothelial cells and a component, components, in the knobs of the infected erythrocytes.

Animals↗
PubMed1981

The development of the normal infantile hip as expressed by radiological measurements.

Acetabular and centre edge angles were measured on normal radiographs of 164 children (328 hips) aged from three months to five years. Using regression and correlation analysis, mathematical formulae were derived which allow the calculation of the normal acetabular and centre edge angles for a given age. The relationship between age, acetabular angle and centre edge angle was studied.

Acetabulum↗
PubMed1981

Presence of autoantibody for phospholipase inhibitory protein, lipomodulin, in patients with rheumatic diseases.

The activity of phospholipase inhibitory protein, lipomodulin, partially purified from rabbit neutrophils, was markedly decreased after treatment with sera from patients with rheumatic diseases such as systemic lupus erythematosus, rheumatoid arthritis, and dermatomyositis. The decrease of the protein's inhibitory activity on phospholipase A2 paralleled the amount of [35S]methionine-labeled lipomodulin precipitated by the sera. Absorption of patients' sera with anti-human IgM (mu chain) or protein A-agarose, but not with anti-human IgG (gamma chain), decreased their ability to decrease the activity of lipomodulin on phospholipase A2 or to precipitate the radioactive lipomodulin. The IgM fraction of patients' sera could precipitate [35S]methionine-labeled lipomodulin (40,000 daltons) which comigrated with highly purified lipomodulin on gel electrophoresis with sodium dodecyl sulfate. All of these observations suggest that the sera of many patients with rheumatic diseases contain autoantibody against lipomodulin. A monoclonal antibody against lipomodulin was also obtained. Stimulating human fibroblasts with bradykinin in the presence of monoclonal antilipomodulin antibody markedly enhanced arachidonic acid release due to the activation of phospholipase(s) in the intact cells, and this stimulatory effect was blocked by adding purified lipomodulin. These findings suggest that lipomodulin regulates the activity of phospholipase(s) on the cell surface and that autoantibodies against lipomodulin may play a role in certain symptoms of rheumatic diseases, especially by the formation of prostaglandins and other metabolites of arachidonic acid.

Animals↗
PubMed1981

Transient cerebral ischaemic attacks--management and prognosis.

Fifty patients who had recently had a transient ischaemic attack took part in a double-blind cross-over trial of sulphinpyrazone 200 mg 4 times daily against placebo. Each treatment was given for 4 months. The incidence of recurrences was much greater in the initial 4 months but there was no difference between the 2 treatments. A follow-up of 39 of the patients showed that 2 years later 90% of those who had not had a recurrence during the 8 months had suffered no further neurological events whereas of those who did have a recurrence during the study only 47% had no further neurological events.

Aged↗
PubMed1981

Antibodies to T cells in patients with systemic lupus erythematosus can induce antibody-dependent cell-mediated cytotoxicity against human T cells.

Patients with active systemic lupus erythematosus (SLE) often have circulating antibodies to T cells. These patients also often have leukopenia and diminished numbers of T lymphocytes. In addition, certain T lymphocyte functions are frequently impaired in patients with SLE. It has been previously considered that a complement-dependent cytotoxic mechanism was responsible for the above observations. We now demonstrate that antibody-dependent cell-mediated cytotoxicity (ADCC), a cytotoxic reaction mediated by antibody and effector cells in the absence of complement, can also kill T cells from normal individuals as well as from patients with SLE. Moreover, this ADCC could be observed using the plasma, effector cells, and target cells all obtained from the same individual with SLE. Plasma of those patients with active SLE, and in whom anti-T cell antibodies could be demonstrated by the more classical complement-dependent cytotoxicity, was most often able to mediate such an ADCC reaction. The IgG fraction of the plasma was responsible for inducing ADCC, and aggregated IgG could block the reaction. The fact that the IgG fraction was often more effective than the unfractionated plasma suggested that immune complexes present in SLE plasma might partially block the expression of ADCC. Because a single SLE plasma could induce ADCC in T cells from several different unrelated individuals, it is unlikely that antibodies directed against particular human leukocyte antigens (HLA) or blood group antigens are involved.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1981

Autologous rosette-forming T cells regulate responses of T cells. Phenotypic and functional analysis of suppressor cells generated from autologous rosette-forming T cells after autologous mixed lymphocyte reactions.

An average of 5--9% of human peripheral blood of T lymphocytes from rosettes with autologous erythrocytes (ARFT). This population responded only slightly against autologous and allogeneic non-T cells. In contrast, T cells that did not form rosettes with autologous erythrocytes (NRFT) proliferated to a greater degree in auto- and allogeneic mixed lymphocyte reactions (MLR) and also in reactions to trinitrophenyl (TNP) modified autologous non-T cells (TNP-auto-MLR) as compared with ARFT or unfractionated T cells. The ARFT populations could suppress the increased allogeneic (allo)MLR and TNP-auto-MLR of NRFT when the ARFT were added to the NRFT at the beginning of the cultures. Fluorescence-activated cell-sorter (FACS) analysis of these freshly obtained T cell fractions using monoclonal antibodies to subpopulations of T cells did not demonstrate any selective gain or less of T cell subsets in the ARFT and NRFT as compared with unfractionated T cells. But when each T cell fraction was cultured separately for a week in the presence of autologous non-T cells (auto-MLR) and the cells were again analyzed by fluorescence-activated cell sorter, there was an increase in OKT8-positive cells (suppressor/cytotoxic subset) only in the ARFT fraction. The above findings strongly suggest that suppressor T cells are generated from the ARFT fraction during an auto-MLR, these may then regulate the responses on NRFT.

Antigens, Surface↗
PubMed1980

Antigen presentation and allogeneic stimulation by Langerhans cells.

Isolated Langerhans cells were studied for 2 immunologic functions, the ability to present antigen to sensitized T lymphocytes and the ability to act as stimulator cells for mixed lymphocyte reactions. Langerhans cells can perform both of these functions. This fact, with the previous finding that Langerhans cells possess surface Ia antigens and Fc and C3 receptors, strongly suggests that Langerhans cells act as epidermal macrophages.

Animals↗
PubMed1980

The functional role of Langerhans cells.

Langerhans cells represent a subpopulation of mammalian epidermal cells. The recent findings that these cells are the only epidermal cells which express Fc-IgG receptors, C3 receptors and Ia antigens support the early suggestion that they are related to cells from the monocyte-macrophage-histiocyte series. In this report, evidence is presented that epidermal Langerhans cell can replace Ia-bearing macrophages in their capacity to induce antigen-specific and allogeneic T cell activation. The possible clinical implications of these findings are discussed with regard to the role of Langerhans cells as sensitizing factors in contact hypersensitivity and skin graft rejection.

Animals↗
PubMed1980

Immunologic characterization of a granulocytic leukemia of inbred strain 13 guinea pigs: presence of Ia-positive myeloblasts.

Membrane markers expressed by a transplantable granulocytic leukemia induced in inbred strain 13 guinea pigs by N-nitroso-N-butylurea have been investigated by serologic and immunochemical methods. Although the leukemic myeloblasts have no detectable surface immunoglobulin or Fc receptors, they have been found to synthesize and express membrane antigens encoded for by the I-region of the major histocompatibility complex. Despite the presence of Ia antigens, these cells do not stimulate allogeneic T lymphocytes in the mixed lymphocyte reaction nor are they able to present soluble antigen to immune T cells. The presence of Ia antigens on immature myeloid cells suggests that these proteins may be important in cellular functions beyond those identified in the cellular immune system.

Animals↗
PubMed1980

The autologous mixed lymphocyte reaction in strains of mice with autoimmune disease.

We have studied the autologous mixed lymphocyte reaction (AMLR) in 3 strains of mice with autoimmune disease. T cell proliferation to autologous non-T cells occurs in young mice of these 3 strains (as it does in normal mice) but is absent or greatly reduced in older mice of strains with autoimmune disease. Reciprocal mixing experiments revealed that the defect in the AMLR of the older mice resides in the responder T cell population. Further analysis of the cells participating in the AMLR of young mice of the B/W F1 strain revealed that: 1) a Thy 1- and Ly1-positive responder cell was necessary at the start of the culture to initiate the AMLR; 2) the cells present after 5 days of culture contained very few, if any, Ly123 cells in the B/W F1 strain compared with the normal C57BL/6 strain; and 3) the stimulating cell appear to be a macrophage, and an Ia-bearing cell must be present for the reaction to occur.

Aging↗