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At least 199 records · Page 11Linked to original sources
PubMed1991

[T lymphocyte activation induced by monoclonal anti-CD3 antibodies: physiopathology of cytokine release].

Anti-CD3 monoclonal antibodies are largely used as therapeutic agents in clinical transplantation. Constrating with their potent immunosuppressive activity anti-CD3 antibodies also transiently express T cell activating properties. In vitro they promote T cell mitogenesis and in vivo, the self-limited cytokine release (including TNF, IFN gamma, IL-2, IL-3, IL-6) observed following the first anti-CD3 injection, is responsible for an acute clinical syndrome. Clinical studies as well as the experimental data obtained in mice, confirmed that TNF plays a fundamental role in the anti-CD3 induced syndrome. The administration of anti-TNF monoclonal antibodies prior to the first anti-CD3 injection prevents the syndrome not only by blocking TNF bioactivity but also, by modulating the circulating levels of the other anti-CD3-induced cytokins. In particular, this model allowed the description of regulatory pathways existing between TNF and IFN gamma, which in turn regulate IL-3 and IL-6 release.

Animals↗
PubMed1991

Registry report: International Society for Heart and Lung Transplantation.

Orthotopic heart transplantation continues to be a highly successful therapy for end-stage cardiac disease. Recent advances have extended the benefits of this procedure to neonatal patients. The number of patients undergoing single- and double-lung transplantation increases steadily and the indications for transplantation are being expanded. Evaluation of the early results indicates that patients undergoing lung transplantation for vascular disease do not fare as well as those undergoing transplantation for parenchymal disease. Presently, the results of retransplantation are far inferior to primary transplantation and require ongoing evaluation.

Adolescent↗
PubMed1991

[T and B lymphocytes and NK cells in hemolytic uremic syndrome].

Hemolytic uremic syndrome (HUS) is a serious problem in Argentina, where 50% of the known cases are reported to come from. In the so-called "typical" HUS, anemia, thrombocytopenia and acute renal failure are usually preceded by an episode of infection. Many agents such as bacteria, toxins and viruses have been linked with the prodromal episode, but the reason for the occurrence of HUS in only a small portion of individuals with identical previous symptoms, is not clear. The hypothesis of a particular immune response modifying the susceptibility of some hosts to develop the syndrome after an otherwise well tolerated infection is not formally excluded. The aim of our work was to explore some immunological parameters in order to add more data concerning the immunologic changes occurring during the acute phase of HUS in 24 pediatric patients. We coincide with previous authors on the normal values of serum complement levels and the increase of IgG, IgA and IgM concentrations. (Table 1). We also report a significant and transient decrease in the percentage of T lymphocytes and an increase in the relative number of B lymphocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

B-Lymphocytes↗
PubMed1991

Human T cell activation by OKT3 is inhibited by a monoclonal antibody to CD44.

The CD44 molecule, also known as Hermes lymphocyte homing receptor, human Pgp-1, and extracellular matrix receptor III, has been shown to play a role in T cell adhesion and activation. Specifically, anti-CD44 mAb block binding of lymphocytes to high endothelial venules, inhibit T cell-E rosetting, and augment T cell proliferation induced by the CD2 or CD3-TCR pathways. We have characterized an anti-CD44 mAb (212.3) which immunoprecipitates a 90-kDa protein and is specific for CD44 as shown by peptide mapping and antibody competition studies. Interestingly, our studies with 212.3 demonstrate that this CD44-specific mAb completely inhibits T cell proliferation stimulated by the anti-CD3 mAb, OKT3. Inhibition is not a result of reduced cell viability, but is associated with 1) inhibition of IL-2 production, 2) inhibition of IL-2R expression, and 3) inhibition of OKT3-mediated increases in intracellular Ca2+ levels. In addition, 212.3 does not inhibit proliferation by the T cell mitogens PHA or PWM nor does it inhibit proliferation in a mixed lymphocyte reaction. Similar to other anti-CD44 mAb, 212.3 also augments T cell proliferation induced by mAb directed against the T11(2) and T11(3) epitopes of CD2. Thus, these studies describe a novel CD44-specific mAb (212.3) that inhibits T cell activation by OKT3 by blocking early signal transduction. Furthermore, these studies suggest that "receptor cross-talk" between the CD3-TCR complex and CD44 may regulate T cell activation.

Animals↗
PubMed1991

[Acute clinical syndrome associated with OKT3 administration. Prevention by single injection of an anti-human TNF monoclonal antibody].

This study analyzed the capacity of an anti-human tumour necrosis factor (TNF) monoclonal antibody, CB006 (murine IgG1, Celltech), to prevent the OKT3-induced acute clinical syndrome. Fourteen renal allograft recipients undergoing prophylactic OKT3 therapy were included. CB006 was administered as a single i.v. injection, 0.4 mg/kg (Group I, 7 patients) and 2 mg/kg (Group II, 7 patients), one hour prior to the first OKT3 administration. Nineteen consecutive patients that were part of a randomized multicenter trial constituted the historical control group. In all patients CB006 was perfectly well tolerated and significantly decreased the frequency of the common OKT3-associated acute symptoms. None of the CB006 pretreated patients showed severe life threatening symptoms (hypotension, respiratory distress or neurotoxicity), observed in 10 per cent of historical controls. At variance with controls, in CB006 treated patients gastrointestinal symptoms (vomiting, diarrhea) and pyrexia (body temperature greater than or equal to 39 degrees C) appeared in low frequency, were mild and short lasting, never promoting major prostration of the patients due to electrolytes and fluid loss. Importantly, the presence in some patients of these mild symptoms, correlated with detectable bioactive TNF in the circulation thus reflecting incomplete blockade by CB006 of OKT3-induced TNF. CB006 pharmacokinetics data further stressed the need for adequate dosage adaptation. CB006 did not affect the biological or clinical effectiveness of OKT3. None of the patients showed evidence of anti-CB006 xeno-sensitization.

Antibodies, Monoclonal↗
PubMed1991

[Antilymphocyte serum, cyclosporine and corticoids, versus OKT3, cyclosporine, and corticoids in kidney transplantation].

UNLABELLED: The use of the antilymphoblast globulin (ALG) or OKT3 associated with cyclosporine (CyA) and steroids has been useful in kidney cadaveric transplantation. 101 patients who received their first cadaveric renal transplant were randomized according to the immunosuppression used. Group A (n = 53): horse ALG 15 mg/kg just before transplant surgery; ALG 12 mg/kg on the first day after transplant followed by 4 doses of 10 mg/kg on alternate days; Cya p.o 8 mg/kg/d; prednisone 0.25 mg/kg/d. Group B (n = 48): OKT3 5 mg just before transplant followed by 4 doses of 5 mg/d.; CyA and prednisone were administered using the same schedule as group A. RESULTS: the incidence of rejection during the first 3 months was: group A: 13 percent, group B: 17 percent (NS). The probability of being free of acute rejection (Kaplan-Meier) 24 months after transplant was 89 percent in group A and 79 percent in group B (NS). The day of onset of the first acute rejection episode was 25 +/- 20 days after transplant in group A, and 17 +/- 10 day in group B (NS). Incidence of tubular necrosis: group A 21 percent, group B 19 percent (NS).

Adrenal Cortex Hormones↗