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F Pratesi

Publications and source records attributed to F Pratesi.

At least 19 recordsLinked to original sources
PubMed2006

Heart- and skeletal muscle-specific antigens recognized by trichinellosis patient sera.

The heart can be seriously affected in human trichinellosis, and cardiac involvement can cause death. Experimental infections in rats have suggested the possible participation of immunopathological processes. The aim of the present paper was to investigate the possible presence in trichinellosis patient sera of antibodies recognizing host tissues and particularly the myocardium. Nineteen sera from late period trichinellosis patients, who acquired infection in the Poznan region (Poland), were tested by immunoblot on extracts from normal rat or human heart ventricle wall, spleen, placenta, kidney and skeletal muscle. Patients' sera recognized several antigens that were not recognized by normal sera. On rat and human heart ventricle wall, a high proportion of sera (42%) reacted with a protein of 68 kDa (P < 0.05 compared to normal sera). The reactivity with this antigen, however, was not significantly different in patients with or without cardiac involvement. When sera were tested on skeletal muscle we found that 47% reacted with a protein of 27 kDa and 53% reacted with a protein of 41 kDa (P < 0.05 for both proteins, compared with normal sera). The reactivity against the 68 kDa antigen and against the 27 and 41 kDa skeletal muscle antigens was not observed on kidney, placenta and spleen extracts. Moreover, very few bands were observed on these tissues as compared to heart and skeletal muscle tissues, thus suggesting a high tissue specificity of the reactivity of trichinellosis sera. In conclusion, this study identifies organ-specific autoantibodies in trichinellosis patient sera, their role in the pathogenesis of cardiac involvement being still unclear.

Adolescent↗
PubMed2005

The immune response to citrullinated antigens in autoimmune diseases.

Post-translational modifications of proteins occur very frequently. One of these modifications, citrullination, is the result of arginine deimination operated by an enzyme, peptidylarginine deiminase (PAD), whose activity is under strict genetic control. Serum antibodies reactive with citrullinated proteins/peptides are a very sensitive and specific marker for rheumatoid arthritis. Genes encoding for PAD enzymes have been investigated in RA: the PADI4 gene confers susceptibility to RA in Japanese patients, but not in Caucasians.

Animals↗
PubMed2004

A family based study shows no association between rheumatoid arthritis and the PADI4 gene in a white French population.

BACKGROUND: Autoantibodies to citrullinated proteins (ACPA) are considered a specific marker for rheumatoid arthritis. Peptidylarginine deiminase (PAD) is the enzyme that converts arginyl into citrullyl residues; different isoforms of the enzyme are expressed in mammals. It has been suggested that the PADI4 gene may contribute to genetic susceptibility to rheumatoid arthritis, but conflicting results have been obtained in different populations. OBJECTIVE: To test the hypothesis that the PADI4 gene may confer susceptibility to rheumatoid arthritis in a white French population, using powerful and highly reliable family based association tests. METHODS: DNA samples were analysed from 100 families where one member was affected by rheumatoid arthritis and both parents were available for sampling. Five single nucleotide polymorphisms, located within the PADI4 gene and in its close proximity, were genotyped by restriction fragment length polymorphism, and haplotypes were constructed. The analysis involved use of the transmission disequilibrium test and genotype relative risk. ACPA were detected by ELISA on cyclic citrullinated peptides and on human deiminated fibrinogen. RESULTS: No single SNP or haplotype was associated with the disease, or was preferentially transmitted. No association was found when patients were partitioned according to ACPA positivity. CONCLUSIONS: No PADI4 haplotype is associated with rheumatoid arthritis in a white French population. The role of genes encoding the other PAD isoforms, or modulating tissue expression or enzyme activity, remains to be elucidated.

Adult↗
PubMed2002

The targets of nephritogenic antibodies in systemic autoimmune disorders.

In situ formation of immune complexes is a well recognized mechanism of renal injury in systemic autoimmune disorders. The identification of intrinsic renal antigens that are targets of nephritogenic antibodies is a field of active investigation. Recently, two proteins expressed in the kidney have been characterized as renal antigens. Alpha-actinin, an actin-binding protein localized in glomerular podocytes, is the major target of nephritogenic anti-DNA antibodies. Alpha-enolase, a glycolytic enzyme, is a target of nephritogenic anti-DNA and non-anti-DNA antibodies.

Actinin↗
PubMed2002

Anti-ribosomal antibodies from lupus patients bind DNA.

Antibodies specific for ribosomal P proteins (anti-P) are a hallmark of systemic lupus as anti-DNA antibodies are. It has been reported that anti-P antibodies are more frequently detected in anti-dsDNA positive sera. The aim of the present study was to verify the binding ability of anti-P antibodies towards polynucleotides and nucleosomes. We purified anti-P antibodies from 8 SLE patients' sera and we analysed them by ELISA on plates coated with DNA or nucleosomes. We performed also inhibition experiments in order to verify the specificity of the binding. All the purified anti-P antibodies bound DNA, but some anti-DNA binding activity remained among the non-anti-P antibodies in the flow through. Only half of the purified antibodies bound to nucleosomes, and anti-nucleosomal activity was demonstrated also in non anti-P antibody fraction. The inhibition experiments performed on two anti-P antibodies pointed out that only the homologous antigen inhibited the binding to either P peptide or DNA coated onto the solid phase. These results show that sera in which the two specificities coexist contain antibodies endowed with a double binding ability for DNA and the P peptide.

Antibodies, Antinuclear↗
PubMed2000

Surface expression of a glycolytic enzyme, alpha-enolase, recognized by autoantibodies in connective tissue disorders.

In systemic autoimmune diseases, autoantibodies specific for alpha-enolase are detected more frequently in patients with active renal involvement. To analyze the properties of anti-alpha-enolase antibodies and the distribution of the enzyme in the cell, mouse monoclonal and polyclonal antibodies were obtained from mice immunized with a glutathione-S-transferase-alpha-enolase fusion protein. Anti-alpha-enolase antibodies were purified from patient sera on enolase from human kidney. Using these antibodies, the distribution of alpha-enolase in the cell was analyzed in subcellular fractions and in the cell membrane by flow cytometry and immunoprecipitation. Plasminogen binding was studied by an immunoenzymatic assay. We observed that alpha-enolase was present in the cytosol and membrane fractions obtained from kidney and U937 cells. By flow cytometry, mouse polyclonal anti-enolase antibodies, one monoclonal and 7/9 human anti-enolase antibodies bound the membrane of U937 cells. One monoclonal antibody and mouse polyclonal anti-enolase antibodies immunoprecipitated a 48-kDa molecule from surface-labeled U937 cells and this molecule was recognized by rabbit anti-enolase antibodies. Both immunization-induced antibodies and 7/9 autoantibodies from patient sera inhibited the binding of plasminogen to alpha-enolase. The results show that alpha-enolase, an autoantigen in connective tissue diseases, is a cytoplasmic enzyme which is also expressed on the cell membrane, with which it is strongly associated. Anti-alpha-enolase autoantibodies isolated from patient sera recognize the membrane-associated form of the enzyme and/or interfere with its receptor function, thus inhibiting the binding of plasminogen. Autoantibodies specific for alpha-enolase could play a pathogenic role, either by a cytopathic effect or by interfering with membrane fibrinolytic activity.

Animals↗
PubMed2000

Autoantibodies specific for alpha-enolase in systemic autoimmune disorders.

OBJECTIVE: To analyze the presence and specificity of anti-alpha-enolase antibodies in various systemic autoimmune diseases. METHODS: Sera from patients with systemic lupus erythematosus (SLE), mixed cryoglobulinemia (MC), systemic sclerosis (SSc), and rheumatoid arthritis (RA) were tested by immunoblot on partially purified a-enolase from human kidney and on beta- and gamma-enolase. The isotype of anti-enolase antibodies was determined by means of isotype-specific monoclonal antibodies. RESULTS: IgG anti-alpha-enolase antibodies were detected in 9/33 (27%) SLE sera (6/9 patients had active renal disease), in 6/19 sera from patients with MC and nephritis, in 0/15 sera from MC patients without renal involvement, in 6/20 (30%) SSc sera, in 2/35 (6%) disease controls with RA, and in 2/32 (6%) healthy controls. The antibodies were not species-specific, but in most cases were specific for the alpha isoform of enolase. The anti-enolase immune response was not isotypically restricted. In half of the patients with SLE the anti-alpha-enolase and anti-DNA antibodies constituted distinct antibody populations, while in the other half a partial overlap of the 2 antibody specificities was observed. CONCLUSION: Anti-alpha-enolase antibodies can frequently be detected in systemic autoimmune disorders. In SLE and MC they are associated with nephritis and in SSc they are associated with severe endothelial damage. Alpha-enolase is ubiquitous, but is highly expressed in the kidney and also on the membrane of several cell types including endothelial cells. Thus, anti-alpha-enolase antibodies could contribute to renal injury not only by the local formation of immune complexes, but also by direct damage to endothelial cells.

Adult↗
PubMed1999

Survey of canine and feline follicular tumours and tumour-like lesions in central Italy.

Between January 1985 and June 1997, a total of 4005 skin biopsies were received from dogs and 898 from cats. Follicular tumours and tumour-like lesions together represented 10.4 per cent and 8.1 per cent of all skin tumours in the dog and cat, respectively. The prevalence of tumour-like lesions, such as follicular and dermoid cysts, dilated pore and focal adnexal dysplasia, was highest, representing 41.2 per cent and 68 per cent of all follicular lesions in dogs and cats, respectively. In the dog, follicular tumours were distributed as follows: trichoblastoma (25.6 per cent of all tumours and tumour-like lesions), infundibular keratinising acanthoma, (14 per cent), pilomatricoma (13 per cent), trichoepithelioma (3.9 per cent) and tricholemmoma (2.3 per cent). In the cat, the distribution was 26 per cent for trichoblastoma, 4 per cent for trichoepithelioma and 2 per cent for pilomatricoma. Tumour-like lesions and infundibular keratinising acanthoma in the dog were mostly located on the trunk, trichoblastoma and tricholemmoma on the head, and pilomatricoma on the neck. In the cat, both tumour-like lesions and trichoblastoma were frequently present on the neck and head.

Animals↗
PubMed1983

Imbalance in T-cell subsets of five children with congenital agammaglobulinemia and its effect on "in vitro" immunoglobulin synthesis.

OKT3, OKT4 and OKT8 monoclonal antibodies have been used to assess the number of total T cells and of some T-cell subpopulations in five children with Congenital Agammaglobulinemia. A significant increase in OKT8+ cells and parallel decrease in OKT4+ cells were observed in all patients, both as percentages and absolute numbers. by contrast there was no significant difference in the number of total T cells (OKT3+) and OKT3+ OKT4- OKT8- cells between patients and controls. Determinations were made of the synthesis of IgG and IgM by normal B cells cultured with T lymphocytes from patients stimulated by pokeweed mitogen. In all cases a significant decrease in Ig synthesis was observed. These results may be consistent with imbalance in the T regulatory subsets. However, a similar imbalance was observed in a healthy father of one patient, who had no other immunological defect. A normal distribution of T-cell subsets was observed in all the other relatives examined.

Agammaglobulinemia↗
PubMed1978

Systolic arterial hypertension and cerebral ischemia.

Systolic arterial hypertension in subjects with regional cerebral ischemia is considered and discussed as regards its frequency and its pathogenetic meaning, and criteria concerning the way of treating it. Systolic arterial hypertension presents a very high frequency in these subjects. At times it is accompanied by moderate diastolic hypertension, to which may be attributed, by way of hypothesis, a compensatory meaning. Considering the pathogenesis of systolic hypertension, the antihypertensive drugs at our disposal do not offer any valid and rational indication. We advance the opinion that a lowering of blood pressure in these subjects may be more harmful than helpful.

Brain Ischemia↗
PubMed1977

Reactive hyperemia in Raynaud's disease.

We studied reactive hyperemia after ischemia, after cold, and after cold plus ischemia, in normal subjects, in fingers with Raynaud's phenomenon, and in fingers without Raynaud's phenomenon in hands where other fingers were affected by Raynaud's phenomenon. The results obtained demonstrate the existence of a criohyperdysestesia both in fingers with Raynaud's phenomenon and in fingers without Raynaud's phenomenon in hands where other fingers are affected by it.

Cold Temperature↗