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Biomedical subjects

F Almerigogna

Publications and source records attributed to F Almerigogna.

54 records · Page 3Linked to original sources
PubMed1985

Phenotypic and functional heterogeneity of human T lymphocytes producing B-cell growth factor(s): a clonal analysis.

Human T cells active on B-cell proliferation are phenotypically and functionally heterogeneous. A series of 43 human T-cell clones, selected according to their ability to release factors active on B-cell proliferation, were analyzed. B-Cell proliferation was evaluated by two different assays, namely, a costimulation assay with anti-mu antibody or by an assay based on B-cell preactivation with Staphylococcus aureus. Eight of these clones expressed the T4-/T8+ phenotype while the remaining were T4+/T8-. The large majority had T-cell growth factor activity as well. However, some clones appeared to have B-cell growth factor activity only. Fourteen clones (eight T8+ and six T4+) also displayed cytolytic activity in a phytohemagglutinin-dependent cytolytic assay.

Antibodies, Anti-Idiotypic↗
PubMed1984

Surface markers and function of circulating thyroid autoantibody-producing cells.

The in vitro synthesis of antithyroglobulin (anti-Tg) and antithyroid microsomal (anti-M) autoantibodies by peripheral blood mononuclear cells (MNC) from patients with autoimmune thyroid diseases was investigated using sensitive immunoradiometric assays. Cultures were carried out in the presence or in the absence of pokeweed mitogen (PWM). Thyroid autoantibodies were undetectable in supernatants of MNC cultures from 9 normal subjects. Supernatants of MNC cultured without PWM had detectable levels of anti-Tg and anti-M in 5 (19.3%) and in 2 (7.7%) of 26 patients with autoimmune thyroid diseases, respectively. In the presence of PWM, a marked increment in the antibody concentrations occurred in all but 1 of these cultures, and the number of positive cultures increased to 13 (50.1%) for anti-Tg and to 15 (57.7%) for anti-M. Studies of MNC fractions depleted of T lymphocytes (non-T cells) were carried out on selected patients showing antibody synthesis only after PWM stimulation. Autoantibody production was not found with non-T cells, but the effect of the mitogen was restored by readdition of T cells. Irradiation (1000 rad) of T cells before coculturing significantly enhanced autoantibody production. With this model no significant functional difference was found between autologous and allogenic T cells from thyroid autoimmune disease patients or from normal subjects. The cells involved in PWM-driven thyroid autoantibody synthesis, as defined by depletion studies, were lymphocytes bearing DR antigens and surface immunoglobulin G (IgG) without detectable surface immunoglobulin M (IgM). Depletion from MNC suspensions of Tg-binding cells abolished PWM-stimulated anti-Tg production, but did not alter the synthesis of anti-M. Further studies were carried out on MNC from a single patient with Hashimoto's thyroiditis, whose non-T cells consistently produced large amounts of anti-M and total IgG in the absence of PWM. The addition of PWM to these unfractionated MNC slightly increased the production of anti-M, but inhibited antibody synthesis after depletion of T lymphocytes. Interestingly, the addition of autologous T lymphocytes to non-T cells inhibited the spontaneous synthesis of anti-M. These data indicate that in vitro synthesis of anti-Tg and anti-M by MNC may be frequently induced by stimulation with PWM in patients with thyroid autoimmune disorders. PWM-stimulated synthesis of thyroid autoantibodies appears to be T-cell dependent and modulated by radiosensitive T lymphocytes. The cells responsible for PWM-dependent thyroid autoantibody synthesis are B lymphocytes with surface membrane IgG and have receptors specific for the autoantigen.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1982

Protein A reactivity of lymphocytes from some patients with chronic lymphocytic leukaemia mediated by an interaction with the F(ab')2 region of surface immunoglobulin.

Peripheral blood lymphocytes (PBL) from 15 of 38 patients with chronic lymphocytic leukaemia (CLL) were capable of forming rosettes with human erythrocytes coated with staphylococcal protein A (SpA-HRBC). PBL from seven patients also showed a marked proliferative response after stimulation with Staphylococcus aureus bacteria strain Cowan I (Cowan Staph). The SpA-rosetting of CLL cells was inhibited by incubation with F(ab')2 fragments of anti-immunoglobulin (Ig) antibodies. In addition, incubation with these fragments inhibited the proliferative response of leukaemic B cells to Cowan Staph. The Cowan-Staph induced proliferation of CLL cells was also impaired by the addition of normal human IgG and human IgG F(ab')2 fragments to the cultures, whereas non-immune rabbit IgG was not inhibitory. The inhibitory activity of human IgG F(ab')2 fragments was retained by a SpA-Sepharose column, and it was found in the material recovered from the same column by acid elution. These data indicate that an interaction between SpA and a structure located in the F(ab')2 region of surface Ig of different classes is responsible for either SpA-binding or the Cowan-Staph-induced proliferative response of PBL from some patients with CLL.

Animals↗
PubMed1982

In vitro production of IgE by human peripheral blood mononuclear cells. III. Demonstration of a circulating IgE-bearing cell involved in the spontaneous IgE biosynthesis.

The presence of surface membrane IgE (SmIgE)-bearing cells in the peripheral blood (PB) of atopic patients was investigated by the use of isotype-specific rosettes of human red blood cells coupled to immunosorbent-purified rabbit or monoclonal mouse antibodies against human IgE (R or M anti-epsilon-HRBC). After dissociation of cell bound IgE by treatment with acid buffer, 2.1 +/- 0.3% and 1.2 +/- 0.3% circulating non-T, non-phagocytic, cells from atopic patients were still capable of forming rosettes with R or M anti-epsilon-HRBC, respectively. IgE molecules detectable on cells after dissociation of cytophilic IgE were quite resistant, like surface membrane IgM (SmIgM), to treatment with proteolytic enzymes, but they were removed under capping conditions by soluble anti-IgE antisera. All SmIgE-bearing (IgE+) cells also bore DR determinants, but many of them lacked SmIgM. Depletion of IgE+ cells strongly reduced the ability of PB lymphocyte suspensions from atopic patients to produce spontaneously IgE protein in vitro. Likewise, depletion of cells bearing DR determinants (DR+ cells) resulted in a marked decrease of the spontaneous IgE biosynthesis, whereas depletion of SmIgM-bearing (IgM+) cells had no effect. These data suggest that cells mainly implicated in the spontaneous IgE production in vitro seen in atopic patients are DR+ IgE+ IgM- circulating lymphocytes.

Antibodies, Monoclonal↗
PubMed1982

In vitro production of IgE by human peripheral blood mononuclear cells. IV. Modulation by allergen of the spontaneous IgE antibody biosynthesis.

Peripheral blood lymphocytes (PBL) from a proportion of grass-sensitive patients, studied during or immediately after the grass pollination period, showed spontaneous production in vitro of grass-specific IgE antibody, whereas PBL from atopic patients sensitive to allergens other than grass pollens or non-atopic individuals did not. Pre-incubation of IgE antibody producing PBL from grass-sensitive patients with minute amounts of a mixed grass pollen (MGP) extract or Rye grass antigen Group I (Rye I) usually resulted in a reduction of the spontaneous production in vitro of IgE protein and in a marked inhibition of the spontaneous production in vitro of grass-specific IgE antibody. This antigen-specific inhibition was not mediated by T lymphocytes, but it was apparently due to a signal directly delivered by antigen to the spontaneously IgE antibody producing cells. The results support the concept that the activity of cells responsible for the persistent IgE antibody formation in vitro in atopic patients can be modulated by antigen.

Antibody Specificity↗
PubMed1981

Surface immunoglobulins are involved in the interaction of protein A with human B cells and in the triggering of B cell proliferation induced by protein A-containing Staphylococcus aureus.

The nature of surface components responsible for the reactivity of a subset of human B cells with staphylococcal protein A (SpA) was studied. The ability of normal non-T cells or non-T cells from patients with chronic lymphocytic leukemia (CLL) to form rosettes with human red blood cells coated with SpA (SpA-HRBC) was strongly inhibited or abolished by incubation with F(ab')2 fragments of antibodies against human immunoglobulin (Ig), whereas the incubation with F(ab')2 fragments of antibodies against a non-Ig cell surface antigen, such as beta 2-microglobulin, had no effect on the SpA-rosetting of human lymphocytes. The role of the reaction between surface Ig (sIg) and SpA in the triggering of the proliferative response induced by Staphylococcus aureus bacteria strain Cowan I (Cowan Staph) on normal or leukemic non-T cells was also investigated. A parallelism was observed between the mitogenic activity on normal human non-T cells of Cowan Staph and F(ab')2 fragments of immunosorbent-purified rabbit antibodies to human mu-chain. On the other hand, monovalent Fab fragments of anti-F(ab')2 or anti-mu chain antibodies were unable to activate human non-T lymphocytes, but usually induced a partial inhibition of the Cowan Staph-induced cell proliferation. Non-T cells from 2 patients with CLL did not respond to either Fab or F(ab')2 fragments of anti-Ig antibodies, but were stimulated to proliferate by Cowan Staph. However, the proliferative response of non-T cells from these patients to Cowan Staph was markedly inhibited or abolished by the addition to the cultures of F(ab')2 fragments of anti-Ig antibodies. Antibody preparations to human F(ab')2 or gamma-chain inhibited the response of IgG-bearing leukemic cells, whereas the Cowan Staph-induced proliferation of IgM-bearing leukemic lymphocytes was inhibited by the addition to the cultures of either anti-F(ab')2 or anti-mu chain antibodies. The proliferative response to Cowan Staph or normal non-T cells was also inhibited by the addition to the cultures of human and guinea pig polyclonal IgG, whereas IgG from other species, such as goat, ox, horse, and rabbit, were poorly or not at all inhibitory. On a molar basis, the F(ab')2 preparation from human IgG was as potent an inhibitor as intact IgG molecules, whereas Fc gamma was much less effective in inhibiting the Cowan Staph-induced cell proliferation. A monoclonal IgM, isolated from the serum of a patient with CLL, whose lymphocytes were able to form rosettes with SpA-HRBC and to proliferate in vitro after stimulation with Cowan Staph, also showed a marked inhibitory activity on the Cowan Staph-induced proliferation or normal non-T cells. These data suggest that an interaction between SpA present on the bacterial cell wall and a structure located in the Fab region of sIg, which is shared by sIgM, sIgG, and perhaps also by sIg of other classes, plays an important role in the triggering of B cell proliferation induced by SpA-containing staphylococci.

Antibodies↗
PubMed1979

A simple solid-phase radioimmunoassay for the measurement of IgG secreted in vitro by human lymphocytes.

A radioimmunoassay is described for measuring IgG, based on the ability of immunoglobulins of this class to inhibit the binding of radioiodinated staphylococcal protein A to IgG linked to a solid phase. The solid phase is represented by ox erythrocytes coated with anti-ox erythrocyte rabbit IgG, a reagent used for detecting cells equipped with receptors for the Fc fragment of IgG. By this assay the IgG secreted in vitro by human peripheral blood lymphocytes stimulated with PWM and those present in samples of very diluted human sera were measured. It was found that the assay is a very rapid, simple and reproducible procedure for the detection of IgG immunoglobulin at the nanogram level.

Animals↗
PubMedDate not supplied

Alterations of both responder T cells and stimulator non-T cells are responsible for abnormal mixed lymphocyte reaction in aged humans.

The autologous and allogeneic mixed lymphocyte reactions of 15 young and 15 aged human adults were compared. Both autologous and allogeneic mixed lymphocyte reactions were significantly reduced in the aged group. T cells from aged adults displayed a reduced proliferative response to non-T cells of either aged or young adults. T cells from young adults also showed a reduced proliferative response to non-T cells from aged adults. Sera from aged adults, showing depression of autologous and allogeneic mixed lymphocyte reaction, did not exert any inhibitory effect on the autologous and allogeneic mixed reaction of lymphocytes from young donors. These data suggest that depression of mixed lymphocyte reaction in aged humans probably reflects intrinsic abnormalities of both responder T cells and stimulatory non-T cells.

Adult↗
PubMedDate not supplied

The Fc epsilon R2/CD23 antigen: a hallmark of chronic lymphocytic leukemia B cells.

The effect of different stimuli on the expression of the low-affinity receptor for the Fc fragment of IgE (Fc epsilon R2/CD23) on peripheral blood B cells from patients with chronic lymphocytic leukemia (CLL) was investigated. CLL B cells cultured for 3 days in medium alone showed a progressive decrease of the Fc epsilon R2/CD23 expression, while the addition to the cell cultures of IgE or interleukin-4 had a slackening effect on the decrease of the Fc epsilon R2/CD23. In contrast, in the presence of interferon-gamma the proportion of Fc epsilon R2/CD23+ cells was more rapidly reduced compared to CLL B cells cultured in medium alone. Stimulation of CLL B cells with Staphylococcus aureus Cowan I (SAC) bacteria, which are able to enhance the expression of Fc epsilon R2/CD23 on normal B cells, induced a rapid loss of the Fc epsilon R2/CD23 from CLL B cells.

Antigens, Differentiation, B-Lymphocyte↗