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Biomedical subjects

M L Gaspar

Publications and source records attributed to M L Gaspar.

31 records · Page 2Linked to original sources
PubMed1989

Proliferation of B cells from chronic lymphocytic leukemia is selectively promoted by B cell growth factor.

B cell activation was studied in B cells from B cell chronic lymphocytic leukemia (B-CLL) patients. After in vitro stimulation, these B cells showed extensive proliferation in the presence of high-molecular-weight B cell growth factor (BCGF). In contrast, this effect was not observed upon addition of recombinant interleukin-2 (IL-2). In agreement, upon stimulation, B cells expressed Bac-1 antigen but failed to acquire the IL-2 receptor. These results demonstrate that the utilization of the BCGF pathway can be segregated from that of IL-2 in B cells from B-CLL patients.

B-Lymphocytes↗
PubMed1988

The B-cell activation pathway in human systemic lupus erythematosus: imbalanced in vitro production of lymphokines and association with serum analytical findings.

Recent knowledge of B-lymphocyte physiology has clarified the role of T cell-derived lymphokines in clonal proliferation and differentiation of B-cell responses. Lymphokine production was analyzed in 19 systemic lupus erythematosus (SLE) patients and sex- and age-matched controls in relation to clinical activity and steroid treatment. When in vitro production of interleukin-2 (IL-2) and B-cell growth factor (BCGF) was tested, both activities were found to be diminished in the group of patients (P less than 0.01), while B-cell differentiation factor (BCDF) activity was higher in this group with respect to normal controls (P less than 0.01). Interestingly enough, this in vitro BCDF synthesis was positively correlated with clinical activity regardless of low-dose steroid treatment. A correlation was also found between BCDF production and the levels of IgG (r = 0.64, P less than 0.01), anti-DNA antibodies (r = 0.52, P less than 0.05), and the IgG/IgM ratio (r = 0.7, P less than 0.01) in serum. Implications of these abnormal T-lymphocyte functions in SLE with respect to in vivo B-cell function are discussed.

Adolescent↗
PubMed1988

Role of interleukin 2 in inducing normalization of natural killer activity in systemic lupus erythematosus.

A low natural killer (NK) activity has been well documented for lymphocytes from systemic lupus erythematosus (SLE) patients. Given the defect in interferon-gamma (IFN-gamma) and interleukin 2 (IL-2) production also reported in SLE, it seemed possible that the absence of these molecules could account for some of the defective NK activity. We have tested the NK activity present in peripheral blood mononuclear cells (PBMC) from SLE patients and its in vitro modulation by different preparations of exogenous IL-2. We have found a low NK activity for PBMC from steroid-treated SLE patients, and we report an enhancement in lytic activity after incubation with mitogen-induced, IL-2-containing supernatants obtained from human tonsils. This increase did not seem to be due to recruitment of new effectors because the numbers of cells expressing NK phenotype (Leu 7+ or Leu 11b+) did not change after the incubation, nor did the target specificity of the lysis. However, a similar degree in the improvement in cytotoxicity was not obtained by incubation with a purified preparation of IFN gamma and/or recombinant IL-2 (rIL-2). A possible role for a molecule other than these lymphokines that might influence this effect is discussed.

Cell Line↗
PubMed1988

Presence of an autoantibody against a Golgi cisternal membrane protein in the serum and cerebrospinal fluid from a patient with idiopathic late onset cerebellar ataxia.

Tissue and cultured cells of different species and embryological origins incubated with serum (diluted up to 10,000-fold) or cerebrospinal fluid (CSF) (6-fold dilution) from a 48-year-old female patient with idiopathic late-onset cerebellar ataxia, exhibited a bright specific perinuclear staining when studied by indirect immunofluorescence microscopy. The pattern of the staining was that characteristic of the Golgi apparatus, consisting of a crescent-shaped juxtanuclear reticulum located in the vicinity of the microtubule organizing center. Changes in location and organization of the organelle stained by the patient's serum during mitosis or after incubation of the cells with Colcemid, taxol or monensin, resulted in a disruption of the reticulum that followed the expected patterns for Golgi apparatus. The staining was specifically absorbed with Golgi cisternae-enriched membrane fractions. Finally, dot-immunoblotting studies of membrane and soluble fractions of Golgi cisternae and vesicles showed that the anti-Golgi antibody (AGA) reacted with the cytoplasmic domain of an integral membrane protein contained in the Golgi cisternae. The presence of this unusual autoantibody in an idiopathic late-onset cerebellar ataxia-bearing patient can afford some insights into the pathogenesis of these neurological diseases.

Autoantibodies↗
PubMed1987

Development of Ly-1+ B cells in immunodeficient CBA/N mice.

Spleen cells from CBA/N mice developing a systemic autoimmune disease after daily injection of CsA during an autologous bone marrow reconstitution were transferred into unmanipulated syngeneic recipients. Adoptive transfer allowed the development of Ly-1+ B cells, which shared Mac-1 differentiation antigen expression with the myelomonocytic lineage. Interestingly, expansion of formerly absent Ly-1+ B cells was paralleled by a severe reduction in common, Ly-1-, B cell development in the recipient. We conclude that precursors for Ly-1+ B lineage do exist in CBA/N mice.

Animals↗
PubMed1987

Selective expansion of a CD3+CD4-CD8- subpopulation in clinical groups associated with human immunodeficiency virus infection.

T lymphocytes (CD3+) without expression of CD4/CD8 surface antigens have recently been described in the thymus and peripheral lymphoid organs. We have conducted a retrospective analysis of the literature, seeking quantitative variations in this T-cell subset in normal heterosexual controls, and in risk, pre-AIDS, and AIDS groups, by means of the subtraction [CD3-(CD4+CD8]) and the ratio 100 X [CD3-(CD4+CD8])/CD3. Dramatic T lymphocytopaenia in AIDS patients and the progressive decay of CD4+ lymphocytes and increase of CD8+ lymphocytes throughout the clinical spectrum of HIV infection have been confirmed. Furthermore, we hereby demonstrate the selective expansion of CD3+CD4-CD8- lymphocytes, directly related to the clinical state in different clinical groups of infected people when compared with controls (P less than 0.05). The inverse relationship between the CD3+CD4-CD8- cell subset and other mature T-cell subsets, mainly CD4+ (r = -0.49; P less than 0.01), suggests the existence of mutual regulatory interactions. These in vivo results, which are in agreement with those obtained in long-term infected cultures, cannot be explained by direct cytopathic effects of the virus on the very few infected cells. Thus, the implication of the expansion of these functional precursors on the prognosis for infected people, and the paradoxes of the immunodeficiency, such as lymphoproliferation and autoimmune features, are discussed.

AIDS-Related Complex↗
PubMed1986

Differential proliferative responses of B cells from BALB/c and autoimmune NZB mice to B-cell growth factor(s).

Highly purified B cells from NZB mice have altered responses to various stimuli which require additional costimulatory signals supplied by factors present in EL-4 supernatants when compared to age-matched control nonautoimmune strains. Both crude preparations of EL-4 supernatants as well as partially purified BSF-p1 induced peak proliferation in B cells from normal strains of mice only in the presence of another stimulatory signal, anti-mu. In contrast, B cells from autoimmune-prone NZB mice proliferated in response to B-cell growth factors, with an age-dependent variation. Splenic B cells from 16- to 22-week-old NZB mice, an age where pronounced autoimmune disease is not observed, demonstrated a near maximum proliferative response with B-cell growth factors alone. While normal B cells responded maximally to BSF-p1 in the presence of anti-mu, B cells from young adult NZB mice (16-22 weeks of age) were not further stimulated to proliferate upon the addition of anti-mu. Such NZB B cells appeared to lack the requirement for a stimulation signal delivered by anti-mu in order to respond to B-cell growth factors. These results suggested that NZB cells were partially activated in vivo in the preautoimmune state so that subliminal triggers lead to full activation.

Animals↗
PubMed1976

Pneumomediastinum following a surgical renal biopsy.

A case of pneumomediastinum, which appeared after a biopsy of the right kidney by minimal lumbotomy, is reported. The anatomicopathological condition of the renal fragment obtained was judged to be focal and segmental hyalinosis. We wish to emphasize the rarity of such a complication, the type of electrocardiographic changes observed, and the rapid and spontaneous recuperation of the patient without further repercussions.

Adult↗