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T M Neri

Publications and source records attributed to T M Neri.

18 recordsLinked to original sources
PubMed1992

T-cell receptor beta-chain gene rearrangement and expression during human thymic ontogenesis.

T-cell receptor (TCR) beta-chain proteins appear early (approximately 15th week of gestation) during human thymic ontogenesis. These beta-chain proteins, which appear before terminal deoxynucleotidyl transferase (TdT), could be an expression of a fully rearranged (V-D-J), incompletely rearranged (D-J), or germline TCR beta-chain gene. The aims of this study, performed from the 15th week onward, were the following: (1) to investigate whether or not TCR beta gene rearranges at an early stage during human thymic ontogenesis; (2) to investigate whether complete presumptive functional (1.3 kb) TCR beta gene transcript is present at these early stages of development, or if incomplete (1 kb) or germ-line (1.1 kb) transcripts are expressed; (3) to examine the phenotype of TCR beta-chain+ cells with two-color fluorescence using monoclonal antibody (MoAb) beta F1 and MoAbs that recognize CD1, CD2, CD3, CD4, CD8, CD5, and CD7 antigens (rabbit anti-calf TdT antiserum was used to detect TdT); and (4) to demonstrate whether or not beta gene N-diversity regions are detectable as early as the 15th week and whether or not N-nucleotide insertions correlate to TdT expression. Fifteen- to 22-week fetal thymuses and pediatric thymuses were investigated. We demonstrated that TCR beta-chain gene rearranged as early as the 15th week in human thymus and that a complete functional TCR beta gene transcript was expressed at these early stages of human development. No other analyses to date have investigated TCR beta gene expression in early human thymus using molecular biology techniques. No significant differences were detectable between phenotypic analysis of fetal and pediatric samples, except for TdT expression, which appeared after the 20th week. Essentially all mCD3+ (OKT3+) cells were beta-chain+ at the different weeks investigated. A significant percentage of CD1+ cells were beta-chain+, and the percentage increased along with the age of development. After the 20th week, we identified three main populations: TdT+, cCD3+, beta F-(early thymic precursors); TdT+, CD1+, beta F1+ (intermediate maturity cortical thymocytes); and TdT-, mCD3+, beta F1++ (mature medullary thymocytes). Given these values, we may consider beta-chain expression an ordered process. beta gene N-nucleotide insertions were correlated to TdT expression, since N-regions increased considerably after the 20th week. A further increase of N-nucleotide insertions was detected from the 22nd week to the 32nd week.

Age Factors↗
PubMed1992

Fine specificity of the human T-cell response to the hepatitis B virus preS1 antigen.

The T-cell response to hepatitis B virus envelope antigens was studied in 11 hepatitis B vaccine recipients; 7 were selected to analyze the fine specificity of the T-cell response to the preS1 antigen. Four distinct T-cell epitopes were identified by peripheral blood lymphomononuclear cell stimulation with a panel of short synthetic peptides covering the preS1 sequence. The immunodominance of the preS1 epitopes included within peptides 21-30 and 29-48 was shown by their capacity to restimulate an HLA class II restricted proliferative response of T cells primed with the whole preS1 antigen. Conversely, peptide-specific T cells selected by peripheral blood lymphomononuclear cell stimulation with peptides 21-30 and 29-48 were able to recognize the native preS1 molecule, confirming that these epitopes are actually generated by the intracellular processing of preS1. Finally, amino acid residues essential for T-cell activation by peptide 21-30 were identified using 10 analogues of the stimulatory peptide containing single alanine substitutions. These results may be relevant to the design of efficient synthetic vaccines against hepatitis B virus infection.

Alanine↗
PubMed1992

Iodine-induced subclinical hypothyroidism in euthyroid subjects with a previous episode of amiodarone-induced thyrotoxicosis.

Amiodarone-induced thyrotoxicosis (AIT) occurs most frequently in patients with underlying thyroid disease and is generally believed to be due to the iodine contamination of amiodarone and iodine released by the metabolism of the drug. We and others have suggested that the thyrotoxicosis may also be secondary to amiodarone-induced thyroiditis. To further determine the etiology of AIT, we administered large doses of iodides [10 drops saturated solution of potassium iodide (SSKI) daily] to 10 euthyroid patients long after an episode of AIT believed to be due at least in part to amiodarone-induced thyroiditis. Six of these 10 patients had an abnormal iodide-perchlorate discharge test before SSKI administration, indicating a subtle defect in the thyroidal organification of iodide. During SSKI administration, 6 patients developed marked iodine-induced basal and/or TRH-stimulated serum TSH elevations, 2 had suppressed basal and TRH-stimulated TSH values, and 2 had normal TSH responses compared to SSKI-treated euthyroid subjects with no history of amiodarone ingestion or thyroid disease. Serum T4 and T3 concentrations remained normal and unchanged during SSKI administration in both the AIT patients and control subjects. These results strongly suggest that excess iodine may not be the cause of the hyperthyroidism associated with amiodarone therapy, especially in those patients with probable amiodarone-induced thyroiditis. Furthermore, like patients with a previous history of subacute thyroiditis and postpartum thyroiditis, the present results suggest that some patients with a previous history of AIT may be at risk to develop hypothyroidism when given excess iodine.

Amiodarone↗
PubMed1979

Fabry's disease with familial lymphedema of the lower limbs. Case report and family study.

The case of a 49-year-old man with Fabry's disease (FD), confirmed by histopathological findings of kidney and skin biopsies and enzymatic studies, is reported. Clinical symptoms mainly consisted in severe neurological involvement, and in conspicuous lymphedema of the lower limbs. Two decreased brothers of the patient were also affected with symptons strongly suggesting FD, as well as the lymphedema of the lower limbs. On the basis of these data, the association of FD with familial lymphedema of the lower limbs is discussed: a lipid accumulation in the lymphatic as well as the blood vessel wall is proposed as a possible explanation; the hypothesis of an inborn error in the development of the lymphatic system, controlled by a gene closedly associated with the FD gene on the same chromosome can also be advanced.

Cerebroside-Sulfatase↗
PubMed1978

[Genetic markers in insulin-dependent juvenile diabetes].

A significant association has been established between insulin-dependent diabetes and HL-A. This was appraised in a selected series of 16 patients and 64 of their first-degree relatives by HL-A typing. The relatives also underwent a glucose tolerance test. The results showed a high incidence of B8 in the patients (31%, VS 15% in controls: p less than 0.01). A previously observed prevalence of Bw 15, however, was not noted. In addition, an increased incidence of Bw 35 was detected (38%, VS 23% in the controls: p less than 0.02). In the case of the relatives, no significant differences in HL-A frequency were apparent, nor could a relationship between HL-A phenotype and altered glucose tolerance be established. The true aetiopathogenetic significance of this association is discussed in the light of recent views concerning HL-A and diseases.

Chromosome Mapping↗
PubMed1978

[Familial Mediterranean fever. Evidence of its autoimmune pathogenesis].

Immunological disturbances in FMF have not been previously reported. In present case, positivity for RA and Waaler-Rose test as well as increase of plasma IgG and IgM immunoglobulins during an episode of acute peritonitis is described. These findings, in association with very high levels of urinary FDP, suggest an autoimmune pathogenesis of the disease.

Acute Kidney Injury↗
PubMed1978

Unusual immunologic findings in familial Mediterranean fever.

Familial Mediterranean fever (FMF) is an inherited disease of unknown etiology. We report a case in which, during an acute febrile attack, rheumatoid factor and immunoglobulin levels rose, and the levels of complement components fell. The level of urinary fibrinogen degradation products also increased, and all results of tests returned to normal at the end of the acute attack. This suggests that an immunologic phenomenon may play a substantial role in the etiology of FMF.

Adult↗
PubMed1977

Clinical, histopathological, and biochemical findings in Fabry's disease. A case report and family study.

An extensive enzymatic and morphological study was performed in a 38-year-old patient with Fabry's disease (FD). The quantitative evaluation of the enzyme alpha-galactosidase was shown to be important in identifying the genetic distribution of FD in the family tree of the patient under study. An enzymatic activity less than 0.5 nanomole/hr/10(6) cells and ranging from 2.2 to 1.1 nanomoles/hr/10(6) cells was found in the affected males and the heterozygous females, respectively. alpha-galactosidase activity in the patient's leukocytes correlates well with the histopathological findings of the kidney and skin biopsy specimens, thus demonstrating the need for both of these special examinations for a correct diagnosis of FD.

Adult↗
PubMed1977

HLA antigens and insulin dependent diabetes mellitus. A family study.

Sixteen insulin dependent diabetic patients (age at onset less than 35 years) and their families were tissue typed for HLA antigens. Glucose tolerance of relatives was also tested. Among diabetic patients two HLA antigens were found with increased frequency: B8 (31 percent, control 15 percent) and Bw35 (38 percent, control 23 percent). Among normal relatives B8 and Bw35 had the same frequency as the control group. Bw15 frequency was not increased in either group. In relatives, no correlation between HLA antigens (B8 or Bw35) and abnormal glucose tolerance, obesity and over-weight at birth was found. Present data confirm previous reports of high B8 frequency in early onset diabetic patients, but fail to demonstrate a raised frequency of abnormal glucose tolerance among relatives bearing B8 (or, in our cases, Bw35). B8 may be considered a genetic indicator for susceptibility to juvenile diabetes. On the basis of present results in families, however non genetic factors clearly also play a determinant role. Furthermore, that diabetogenesis arises from a link between Ir-genes and HLA-B8 antigen should only be considered a suggestive hypothesis.

Adult↗