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Biomedical subjects

C Arcangeli

Publications and source records attributed to C Arcangeli.

At least 37 records · Page 2Linked to original sources
PubMed1989

Activation of cord T lymphocytes. I. Evidence for a defective T cell mitogenesis induced through the CD2 molecule.

A study was carried out on cord blood T cell activation via the CD2-mediated pathway. Despite similar percentages of circulating CD3+ and CD2+ cells in adult and cord blood, the proliferation of cord PBMC to the anti-CD3 mAb and cord T cells to anti-CD2 mAb were defective. The T cell CD3-surface structure was normally able to control CD2-mediated activation, as its modulation by a non-mitogenic anti-CD3 mAb blocked cord PBMC proliferation induced by anti-CD2 mAb. CD2-stimulated cord T cells did not proliferate and did not produce a significant amount of IL-2 in culture, although they expressed the IL-2R. This observation was confirmed by the optimal proliferation of CD2-induced cord T cells when rIL-2 was added. Despite the alternative T cell activation pathway is monocyte-independent in adults, the defective cord T cell activation via the CD2 molecule could also be bypassed by the addition of PMA, small amounts of either autologous or allogeneic adult and cord AC or simply rIL-1 alone. Our findings provide evidence for an intrinsic functional defect in cord CD2-mediated T cell activation, which is linked to an impaired increase of free cytoplasmic calcium, as confirmed by the effectiveness of calcium ionophore A23187 in restoring a good CD2-induced cord T cell proliferation and by measurement of cellular calcium uptake after activation via the CD2 molecule. The characteristics of cord T cells revealed by this study recall the thymocyte functional pattern and may represent functional expression of the previously described phenotypic immaturity of cord T cells.

Antibodies, Monoclonal↗
PubMed1989

T-cell response to anti-CD2 monoclonal antibodies in Down's syndrome.

Peripheral blood mononuclear cells from 10 subjects with cytogenetically documented Down's syndrome (DS) and from 10 age- and sex-matched healthy controls were assayed for their ability to proliferate in response to phytohaemagglutinin, anti-CD3 (OKT3), or anti-CD2 (T11(2) plus T11(3] monoclonal antibodies. Interleukin 2 (IL-2) receptor expression and IL-2 production in mitogen-pulsed lymphocyte cultures was also investigated in parallel. DS cells responded poorly to all the blastogenic stimuli used in this study. Under certain experimental conditions (anti-CD3 or anti-CD2 antibody stimulation), the patients' lymphocytes expressed low levels of IL-2 surface receptors and failed to produce normal amounts of this lymphokine. Studies are currently in progress in our laboratories to determine whether these defects are due to an impairment of the early signalling events surrounding the complexing of CD3, CD2, or lectin receptors to their respective ligands.

Adolescent↗
PubMed1989

T-cell response to phorbol ester PMA and calcium ionophore A23187 in Down's syndrome.

The proliferative response of purified T cells to anti-CD2 monoclonal antibodies (T112 plus T113) was found to be markedly reduced in 12 subjects with Down's syndrome (DS). The addition of phorbol ester PMA, which activates Ca2+/phospholipid-dependent enzyme protein kinase C, or calcium ionophore A23187, which increases intracytosolic free Ca2+ concentration, enhanced, but did not normalize, the defective anti-CD2-mediated T-cell mitogenesis. In contrast, the proliferation of resting lymphocytes from trisomic patients was comparable to that of the control cells when PMA and A23187 were used as co-blastogenic reagents. Because PMA and A23187 together bypass the early activation pathways and promote T-cell growth through the direct induction of membrane interleukin 2 (IL-2) receptor expression and IL-2 synthesis and secretion, it could reasonably be hypothesized that the faulty DS T-cell activation induced by antigen or mitogen is due to a deranged transmembrane signal transduction, rather than a defect in the later intracellular events.

Adolescent↗
PubMed1987

T cell response to anti-CD3 antibody in Down's syndrome.

The non-specific mitogen phytohaemagglutinin (PHA) and an anti-CD3 (OKT3) monoclonal antibody were used to measure the lymphocyte proliferative response in blood samples from 15 subjects with Down's syndrome. Blood from 15 healthy controls closely matched for age and sex was also assayed. The mean blastogenic value in PHA stimulated patient lymphocyte cultures was similar to that calculated in the controls. In contrast, the mitogenic response of lymphocytes from patients with Down's syndrome to anti-CD3 stimulation was on average significantly reduced. Immunofluorescence studies and additional experiments carried out by using semiallogeneic (maternal) monocytes as a source of antigen presenting cells showed that the impaired anti-CD3 induced mitogenesis in Down's syndrome could not be ascribed either to a lack of binding of the antibody to the trisomic cells, or to a defective monocyte-T cell interaction. These findings help to explain the cellular basis of the immune defect in Down's syndrome.

Adolescent↗
PubMed1984

Occult thyrotoxicosis in patients with chronic and paroxysmal isolated atrial fibrillation.

Thyroid function tests, including thyrotropin releasing hormone administration (TRH), were performed in 40 consecutive patients with isolated atrial fibrillation (IAF) (i.e., without any other evidence of cardiac disease). The arrhythmia was chronic in 5 and paroxysmal in 35 patients. Thyrotoxicosis could not be diagnosed either clinically or by abnormal serum levels of T4, T3, T3 BC, and thyroid stimulating hormone (TSH). Thyroid stimulating hormone response to TRH, which was normal in 35 patients, was absent in 5 (12.5%) who were considered to have occult thyrotoxicosis. One had chronic and the other 4 had paroxysmal IAF. The arrhythmia did not recur after antithyroid treatment in these four patients who were in sinus rhythm after a mean follow-up period of 21 months. Full exploration of the thyroid function therefore seems useful not only in patients with chronic IAF, but also in those affected by the paroxysmal form.

Adult↗
PubMed1979

Assessment of sinus node function in asymptomatic subjects with sinus bradycardia and in symptomatic patients with sino-atrial disease.

Sinus node function was evaluated in 18 patients with sinus bradycardia without complaints (Group I), in 16 patients with sinus bradycardia and/or sinoatrial block with complaints (subgroup IIa) and in 14 patients with the bradycardia-tachycardia syndrome (subgroup IIb). Mean values of corrected sinus node recovery time (CSRT), atrial effective refractory period (AERP) and atrial functional refractory period (AFRP) differentiated significatively asymptomatic subjects of group I from the two subgroups of patients with sinoatrial disease, but failed to differentiate each subgroup from the other one. There was no significative difference in mean sinoatrial conduction time (SACT) between group I and each of the two subgroups. Three patients of subgroup IIa and 1 patient of subgroup IIb had a false negative response after both overdrive and premature programmed atrial pacing. Spontaneous cycle length was directly correlated with the sinus node recovery time and the atrial refractoriness in group I, and with the only sinus node recovery time in subgroup IIb. No direct correlations were observed in subgroup IIa. This suggests a less disturbed sinus node automaticity in bradycardia-tachycardia syndrome.

Arrhythmia, Sinus↗
PubMed1976

[Hemodynamic research and physiopathologic remarks on "vibration angiopathy" with Raynaud's phenomenon (author's transl)].

A hemodynamic research was carried out by the authors in ten patients affected with upper limb "vibration angiopathy", as well as in ten healthy control subjects. Digital artery flow and systolic, diastolic and mean pressures were measured, and vascular resistances and the so-called "systolic index" calculated, both in basal condition and following hand warming. In patients with "vibration angiopathy" fingers were examined, which on a previous arteriographic study showed the most and the least severe arterial lesions, respectively. No statistically significant differences were detected between the mean values of the hemodynamic indices obtained from the most and the least involved fingers, respectively, as well as between such values and the control subject ones. These results would suggest--even with due reservation on account of the relatively small number of cases and of their different features--that digital artery lesions, as shown by arteriography, have no definite hemodynamic significance. The lack of a statistically significant decrease of the digital artery mean pressure, compared to control subjects, supports the hypothesis that Raynaud's phenomenon in "vibration angiopathy" is not due to a transmural pressure fall. Finally, the lack of correlation between the severity of arterial lesions and Raynaud's phenomenon site suggests that the vasomotion impairment which causes the phenomenon is not related to such lesions.

Arteries↗
PubMedDate not supplied

Interferon-gamma (r-IFN-gamma) induced activation of alveolar macrophages (AM) from anergic patients with chronic obstructive pulmonary disease (COPD).

Forty-six anergic patients (37 males and 9 females, age range 55-79 yr) were selected from ninety-one patients suffering from COPD due to frequent exacerbations and impaired delayed cutaneous reactivity (43.9%). The phenotype of circulating lymphocytes, their proliferative response to a panel of polyclonal T-cell activators and the candidacidal activity (CA) of circulating PMNs (polymorphonuclear cells) were measured. In 13 patients presenting a defective CA of circulating PMNs, the in vitro response of alveolar macrophage CA to r-IFN-gamma was also determined. We found: 1) a significant reduction in the CL response to PHA in COPD patients vs controls; 2) a low PMN-CA in 23 (57%) COPD patients; 3) a non-significant difference in phenotype analysis in patients and controls; 4) lower CA of AMs in COPD patients than in controls; 5) restoration in vitro of CA by r-IFN-gamma in the group of anergic COPD patients presenting depressed CA. We conclude that a defective cell-mediated immunity could be the basis of the enhanced susceptibility to infectious exacerbations in many COPD patients and that, in vitro, it could be reversed by r-IFN-gamma treatment.

Aged↗
PubMedDate not supplied

Anti-CD3 and anti-CD2-induced T-cell activation in primary Sjögren's syndrome.

Because T-cell dysfunctions have been reported in patients with primary Sjögren's syndrome (SS), peripheral blood mononuclear cell (PBMC) proliferation obtained with anti-CD3 and anti-CD2 monoclonal antibodies was evaluated in these patients. Anti-CD3-induced mitogenesis, which varied widely among the patients, was lower in subjects with evidence of anti-SSA and anti-SSB antibodies than in controls. Moreover, the anti-CD2-induced response was depressed in about half the patients and the nonresponders were mainly those with anti-SSA and anti-SSB antibodies. Phorbol myristate acetate, a protein kinase C activator, used alone or added to anti-CD3, induced greater proliferation in patients than in control PBMC. In contrast, exogenous recombinant interleukin 2 (rIL-2) did not significantly enhance the anti-CD2-induced response of patients' PBMC, as it did in normal PBMC. Peripheral blood and parotid T cells from a patient with well-defined primary SS and parotid enlargement also responded poorly to anti-CD2 stimulation. Exogenous rIL-2 restored T-cell proliferation only in the salivary gland cultures of this patient. The present findings suggest that there is a T-cell activation defect in subjects with primary SS, particularly in those with circulating anti-SSA and anti-SSB antibodies. In addition, the difference in the response to IL-2 of peripheral blood and parotid-infiltrating T cells would seem to indicate that T-cell subsets are differently distributed in the blood and inflammation site.

Adult↗