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T Gallart

Publications and source records attributed to T Gallart.

At least 19 recordsLinked to original sources
PubMed1992

Impaired post-transcriptional expression of interleukin-2 receptor in pokeweed mitogen-activated T cells.

The expression and role of interleukin-2/interleukin-2 receptor (IL-2/IL-2R) system in the pokeweed mitogen (PWM)-induced T cell mitogenesis was studied. In the absence of monocytes (Mo), both soluble and Sepharose-bound PWM fail to induce T cell mitogenesis even when exogenous IL-2 or IL-1 or IL-1 + IL-2 or IL-4 are also present. In the presence of Mo, PWM stimulation of T lymphocytes (highly depleted of B lymphocytes) induces as much IL-2 mRNA as phytohemagglutinin (PHA), but results in higher and persistent IL-2 levels in culture supernatants despite the concomitant T cell mitogenesis, suggesting that PWM-activated T cells do not utilize the IL-2 they produce. Confirming this notion, Mo-dependent PWM-preactivated T cells, as compared to PHA-preactivated ones: (a) failed to consume exogenous IL-2 and their mitogenic response did not increase upon exposure to exogenous IL-2; (b) exhibited very low numbers of high-affinity IL-2R; and (c) showed lower expression of IL-2R p55 and undetectable expression of IL-2R p75 on their surface. Moreover, the PWM-induced T cell mitogenesis was not inhibited by anti-IL-2 or CD25 antibodies and only partially (50%-60%) inhibited by cyclosporin A, while these treatments abrogated the PHA-induced one. PWM-activated T cells, as compared to the PHA-activated ones, exhibited as high (p55) or even higher (p75) mRNA expression of both IL-2R p55 and p75 subunits. The possibility that PWM interferes with IL-2R subunits once expressed on the T cell surface was excluded. Thus, intracellular PWM-related events are likely to impair IL-2R expression post-transcriptionally. Possible explanations for this effect and its relation with the capacity of PWM to induce T cell-dependent B cell differentiation are discussed.

Cyclosporine↗
PubMed1992

Analysis of islet cell antibodies reactivity to a human islet cell line.

A human pancreatic beta cell line (HP62) was tested for reactivity with islet cell antibodies (ICA) as compared with previously-established methods. Using indirect immunofluorescence test, we found that HP62 cell line failed to react in a specific way with ICA from type 1 (insulin-dependent) diabetic patients since sera from normal controls showed a reactivity similar to that found in the patients. So, the usefulness of this human beta cell line as a tool of immunological purpose is questioned when indirect immunofluorescence procedures are used.

Autoantibodies↗
PubMed1991

Stimulation through the TCR/CD3 complex up-regulates the CD2 surface expression on human T lymphocytes.

Despite the well known interrelationship between the CD2- and CD3-mediated signal transduction pathways, it is not well established whether the CD2 surface expression can be regulated by triggering of TCR/CD3 complex. In this study we show that the stimulation of human PBMC with the Cris-7 (CD3) mAb, both in soluble and particulate form, results in hyperexpression of the CD2 surface Ag, as assessed by immunofluorescence and semi-quantitative immunoprecipitation assays. Similar effects on CD2 surface expression were obtained when different CD3 mAb (OKT3, RW2-8C8 and Leu-4) were tested. The CD3-mediated CD2 up-regulation was suppressed by cycloheximide and actinomycin D, indicating that it requires de novo protein and RNA synthesis. In agreement with this, increased CD2 RNA levels were observed after 3 h of stimulation, reaching a plateau at 24 h that was maintained for 72 h. The CD2 up-regulation was concomitant to other CD3-induced activation-related events such as induction of surface CD25 and CD71 and high RNA levels for c-myc, IL-2R alpha- and beta-chains, CD71, and IFN-gamma. CD2 up-regulation appeared to be elicited by a protein kinase C-dependent mechanism because it was abrogated by staurosporine, a potent protein kinase C inhibitor. Moreover, IL-2-dependent events may also help in enhancing CD2 hyper-expression because it was only partially inhibitable by cyclosporine, dexamethasone, or Mar-108 (CD25) mAb. In conclusion, our data suggest that CD2 up-regulation can be a relevant event in T cell activation triggered by the physiologic engagement of the TCR/CD3 complex.

Antibodies, Monoclonal↗
PubMed1991

Increased CD5-positive B lymphocytes in type I diabetes.

CD5+ B lymphocytes have been implicated in the production of polyspecific and monospecific antibodies that bind self-antigens, and increased proportions of this B cell subset occur in patients with some autoimmune diseases. We investigated the proportion of peripheral blood CD5+ B lymphocytes in type I diabetic patients. Compared with 18 age-matched healthy subjects, 11 out of 28 (39.2%) type I diabetic patients had increased proportions of circulating CD5. B lymphocytes with no alterations in the numbers of circulating B and T lymphocytes. Although all patients with increased CD5 B lymphocytes also had serum islet cell antibodies and/or insulin autoantibodies, the occurrence of increased proportions of CD5+ B lymphocytes and serum autoantibodies was not significantly correlated. Increased proportions of CD5+ B lymphocytes was not related to the time elapsed since the clinical onset of diabetes. In addition, regardless of being increased or normal, the proportion of CD5+ B lymphocytes appeared as a relatively constant phenotype after 1 year of follow-up studies at 3-month intervals in eight patients. Although the significance of these findings remains to be established, the possibility exists that CD5+ cells play a role in the pathogenesis of type I diabetes.

Adolescent↗
PubMed1991

Serum levels of secretory IgA in ankylosing spondylitis.

An ELISA test was performed in order to measure the serum levels of secretory IgA (sIgA) in 51 patients with ankylosing spondylitis (AS) and 30 healthy controls. Raised values of sIgA were found in AS patients compared to controls. Patients with active disease, defined by clinical criteria, showed a significant elevation of serum sIgA compared to healthy controls (p = 0.03) or to patients with inactive disease (p = 0.02). A positive correlation between total serum IgA and sIgA was found (p = 0.001). Our findings further support the role of the mucosal stimulation in the pathogenesis of AS.

C-Reactive Protein↗
PubMed1990

Phosphorylation-mediated changes in the electrophoretic mobility of CD5 molecules.

This work shows that tumor promoter agents (TPA) induce the post-translational modification of the human lymphocyte surface CD5 antigen (Tp67) in several cellular types. Treatment of [32P]orthophosphate- and [35S]cysteine-labeled normal and lymphoblastoid T and B cells with active tumor promoters induced the rapid, transitory and dose-dependent appearance of hyperphosphorylated CD5 forms with higher apparent molecular masses. These changes in the electrophoretic mobility of CD5 molecules were independent of RNA and protein synthesis, as well as of differences in neuraminic acid content. The inhibition of the TPA-mediated changes by protein kinase C inhibitors (staurosporine and 1-(5-isoquinolylsulfonyl)-2-methylpiperazine) indicated its protein-kinase-C-mediated nature. Phosphatase digestion of CD5 immunoprecipitates reverted the TPA-mediated mobility changes showing its dependence on phosphorylation. Neuraminidase digestion of intact cells revealed that the target of the TPA effects are surface-expressed CD5 molecules. In conclusion, we suggest that the heterogeneity in the electrophoretic mobility induced by TPA could reflect some structural and/or functional differences within CD5 molecules.

Antigens, Differentiation↗
PubMed1990

Protein kinase C-dependent up-regulation of CD5 surface expression on normal and lymphoblastoid T cells.

As an approach to study the mechanisms regulating the surface expression of CD5 antigen on T cells, the effects of agents that activate different lymphocyte functions were examined. Active tumour promoter agents (TPA), such as phorbol ester analogues [phorbol 12-myristate 13-acetate (PMA), phorbol 12, 13-dibutyrate (PBu2)] and mezerein, were able to increase the expression of CD5 on the cell surface of all T-cell lines), as deduced from immunofluorescence and immunoprecipitation analysis. The TPA-induced CD5 up-regulation occurred in a dose-and time-dependent manner and was dependent on protein and RNA synthesis. From the other stimuli tested, the T-cell mitogens [phytohaemagglutinin (PHA) and concanavalin A (Con A)], as well as monoclonal antibodies (mAb) against the CD3 complex, also increased CD5 expression, although to a lesser degree. In all cases the increments were shown to be dependent on protein kinase C (PKC), as evidenced by their inhibition with staurosporine, a potent inhibitor of PKC activation. These data suggest that CD5 up-regulation on T cells can be a physiological event that depends on PKC activation.

Antigens, Differentiation↗
PubMed1989

Cellular activation without proliferation to B cell growth factor and interleukin 2 in chronic lymphocytic leukaemia B cells stimulated with phorbol ester plus calcium ionophore.

Individual leukaemic B cells of chronic lymphocytic leukaemia (CLL) do not proliferate to B cell growth factor (BCGF) or interleukin 2 (IL-2) when co-stimulated with immunoglobulin (Ig) ligands. To exclude possible defective signalling via surface Ig (sIg), phorbol myristate acetate (PMA) plus calcium ionophore (A23187) were used to activate purified CLL B cells and compared with staphylococcal protein A coupled to sepharose beads (Seph-PA). RNA synthesis and phenotypic changes after PMA plus A23187 stimulation indicate that CLL B cells from (10) different individuals are similarly able to undergo the G0 to the G1 phase transition and express surface activation antigens. In contrast, they are variable in the capacity to show DNA synthesis, which occurred in only six out of 10 cases. Even in the presence of BCGF (10%, v/v) or IL-2 (50 U/ml) four out of nine CLL B cells activated with PMA plus A23187 or PMA alone were still unable to proliferate although they were induced to express CD23, 4F2, CD25 and OKT9 antigens by PMA plus A23187. However, PMA plus A23187 induced IgM secretion which increased further in response to IL-2 even in the absence of DNA synthesis. Moreover, in other CLL B cell populations, the unresponsiveness to growth factors upon co-stimulation with Ig ligands (Seph-PA) may simply reflect a defective signalling via sIg cross-linking which can be circumvented by PMA plus A23187 stimulation. Recombinant Interferon-gamma (50 U/ml) failed to affect DNA synthesis and IgM secretion.

B-Lymphocytes↗
PubMed1989

Differential responsiveness of human B lymphocytes to phorbol ester and calcium ionophore based on their state of activation.

For tonsil B cells of a particular high density (below 65% Percoll), both phorbol myristate acetate (PMA) (5 ng/ml) and calcium ionophore A23187 (500 nM) were required to induce RNA synthesis, significant DNA synthesis also occurring in the presence of 12,000 MW B-cell growth factor (BCGF). In contrast, PMA alone, even at 1 ng/ml, was a sufficient stimulus to induce strong DNA synthesis in low-density B cells (45-50% Percoll) and strong proliferative responsiveness to BCGF in intermediate-density B cells (55-65% Percoll). In these latter B-cell populations, A23187 (500 nM), acted synergistically with non-mitogenic PMA doses to induce strong DNA synthesis, the PMA dose required being 5-50 times lower in low-density B cells (0.1-1 ng/ml) than in intermediate-density B cells (5 ng/ml). Preactivation for 30 hr with anti-Ig antibodies plus BCGF, known to drive B cells into late G1, rendered high-density B cells responsive to PMA (1-10 ng/ml) with high, dose-related DNA synthesis. These data indicate that the B-cell mitogenicity of a given nanomolar dose of PMA depends on the more advanced state of activation of B cells. It was also found that the above optimal dose of A23187 (500 nM) paradoxically inhibited the PMA-induced DNA synthesis of low-density B cells and in vitro preactivated high-density B cells. Data obtained with low-density B cells suggest that a calcium influx during the PMA-induced proliferative phase of B cells may provide a negative signal for the DNA synthesis.

B-Lymphocytes↗
PubMed1988

Combined assay of adenosine deaminase, purine nucleoside phosphorylase, and lactate dehydrogenase in the early clinical evaluation of B-chronic lymphocytic leukemia.

The levels of adenosine deaminase (ADA), purine nucleoside phosphorylase (PNP), lactic dehydrogenase (LDH), and LDH isoenzyme patterns (LD1 to LD5) have been measured in lymphocyte extract from 28 patients with B-chronic lymphocytic leukemia (B-CLL). The activities of ADA, PNP, and LDH have been correlated with two morphological groups of B-CLL classified according to the percentage of large, nongranular, atypical lymphocytes (AL) in peripheral blood: "typical" B-CLL (less than 10% of AL, 21 cases) and "atypical" B-CLL (10-25% of AL, seven cases). Patients with atypical B-CLL had significantly (P less than 0.001) higher activities of ADA (0.46 +/- 0.17 U/10(9) cells), PNP (1.74 +/- 1.0 U/10(9) cells), and LDH (48.3 +/- 9.7 U/10(9) cells) than patients with typical B-CLL (ADA, 0.29 +/- 0.1 U/10(9) cells; PNP, 0.58 +/- 0.23 U/10(9) cells; and LDH, 29 +/- 10 U/10(9) cells). In addition, the "treatment-free period" was also significantly (P less than 0.025) shorter in the group of atypical B-CLL compared with the typical B-CLL group. No clear-cut statistical differences in lymphocyte surface markers or in several other prognostic factors between the two subgroups of B-CLL were found. The present study supports the idea that in B-CLL the simultaneous determination of ADA, PNP, and LDH might be helpful in better understanding the pathophysiology, prognosis, and natural history of the disease.

Adenosine Deaminase↗
PubMed1988

Recombinant alpha 2-interferon in the treatment of B chronic lymphocytic leukemia in early stages.

Ten previously untreated patients with early B cell chronic lymphocytic leukemia (B-CLL) (seven in Rai's stage 0, three in stage I) were given recombinant alpha 2-interferon (alpha 2IF) (2 X 10(6) U/m2 intramuscularly three times a week for a minimum of 14 weeks) to assess its effectiveness. All patients were evaluable for response to therapy and toxicity. No complete response was achieved. In all cases a definite, although transient reduction in the absolute number of peripheral blood lymphocytes was observed. In eight patients an increase in the absolute number of granulocytes was detected. None of the patients experienced severe hematologic toxicity. Fatigue, malaise, and fever were the more common side effects, but all patients were able to finish their treatment as planned. The results of this pilot study suggest that low doses of recombinant alpha 2-IF have some activity in early and previously untreated B-CLL and that further studies of IF effectiveness in B-CLL seem warranted.

Adult↗
PubMed1987

Transient immunologic defect in a case of Listeria rhombencephalitis.

We report a case of Listeria rhombencephalitis in a previously healthy 60-year-old man. Listeria rhombencephalitis is a rare but well-defined clinical syndrome of lower brain-stem involvement caused by Listeria monocytogenes. Contrary to other listerioses, rhombencephalitis has been mainly observed in patients without predisposing conditions. In our case, however, findings of a detailed immunologic study, performed three months and one year, respectively, after clinical onset of Listeria rhombencephalitis manifestations, showed a transient cellular immunity defect, not associated with any other apparent disease.

Encephalitis↗
PubMed1987

"Spontaneous" complete remissions in chronic lymphocytic leukemia: report of three cases and review of the literature.

"Spontaneous" complete remissions (SCR) are a rare event in chronic lymphocytic leukemia (CLL). In this article, we report three cases of SCR observed in a series of 285 patients followed at a single institution during the last 15 years. SCR was documented by clinical and hematologic data, including bone marrow biopsy, and immune cell markers. A delay of 0.9-1.6 years between "clinical" and "clonal" remission was observed. A review of other cases of SCR in CLL is also performed.

Aged↗
PubMed1986

Cellular infiltrate in renal graft rejection: T lymphocyte subsets detected by monoclonal antibodies.

We have examined the interstitial cellular infiltrate using monoclonal antibodies against T cells (Cris 1), helper/inducer T cells (OKT4) and suppressor/cytotoxic T cells (OKT8) by indirect immunofluorescence in renal biopsies taken from 14 transplanted patients during clinical episodes suggestive of acute (n = 9), chronic (n = 2) and no rejection (n = 3). Infiltrating T cells and T cell subsets were found to be significantly increased during all types of rejection (n = 11) as compared to no rejection (n = 3). Two types of biopsies could be distinguished according to the predominance of T cell subsets. In some biopsies (n = 6), OKT8+ cells were significantly more numerous that OKT4+ cells. In the remaining biopsies (n = 5), OKT4+ cells were more common that OKT8+ cells, the OKT4/OKT8 ratio being significantly higher. No association was observed between HLA mismatch and predominating T cell subset, neither for type nor outcome of graft rejection. Our results suggest that the OKT4+ cells may play a more important role than previously reported in renal graft rejection.

Adolescent↗
PubMed1986

Lymphocyte subpopulations in Spanish parenteral drug addicts.

Lymphocyte subpopulations were studied in 29 symptom-free Spanish prisoners who were active parenteral drug abusers. In 16/29 drug addicts (55%) the helper-inducer/suppressor-cytotoxic ratio (Leu 3a/Leu 2a) was less than 1. None of these 16 patients had lymphopenia and only 2 had a reduction in the number of Leu 3a cells. In drug addicts the number of lymphocytes (p less than 0.01) and the number and percentage of Leu 2a cells (p less than 0.001) were significantly raised. The addicts also had a higher absolute number of T cells when measured by their ability to react with the Leu 4 antibody (p less than 0.01). However, the E-rosette forming cells were significantly reduced. Thus the E-rosette test may lead to an overestimation of "null" cells. Furthermore drug addicts had a higher percentage (p less than 0.001) of Leu 7 positive cells (NK and K cells), but a normal percentage of B and phagocytic cells. Five drug addicts had generalized persistent lymphadenopathies, and 2 had skin anergy. We believe that most of the immunologic abnormalities seen in these apparently healthy drug abusers can be explained by an antigenic overload.

Adolescent↗