These studies were carried out to examine the presence of the inflammatory cytokines IL-6 and TNFalpha in kidneys of patients with lupus nephritis as an indicator of their possible role in its pathogenesis. A total of 19 kidney biopsies from patients with type III or IV lupus nephritis were processed by direct immunofluorescence using monoclonal anti-IL-6 and TNFalpha antibodies. Local expression of these genes was demonstrated both by in situ hybridization and by reverse transcriptase-PCR amplification of total RNA isolated from kidney tissue. Fifty-two percent of the biopsies exhibited IL-6 and TNFalpha deposited along the glomeruli and tubules; in situ expression of these cytokines was demonstrated in 6 biopsies with type IV, and 1 with type III nephritis. Inflammatory cytokines are actively synthesized in the kidneys of patients with lupus nephritis and therefore, may play a role in its pathogenesis.

Serum hsa-miRs 512-3p, 518f-3p, 520c-3p, and 520d-3p, are differentially expressed between WWD-PE and controls and their role in the development of preeclampsia should be investigated further.

No abstract

The purpose of this study was to determine whether phosphorylation has an effect on the characteristics of the 60 kD Ro antigen throughout the cell cycle. Cell extracts of synchronized HEp-2 cells were phosphorylated in vitro with exogenous ATP, examined by SDS-PAGE and Western blot, and probed with specific anti-Ro sera. In addition, cellular ATP pools were radiolabelled in vivo with 32P. The presence of the Ro protein was detected with a molecular weight of 60 kD during all phases of the cell cycle, except at the M phase, where it was increased to 65 kD. Phosphorylation of the in vitro and in vivo cell extracts increased the molecular mass to 65 kD. Moreover immunoprecipitation assays demonstrated that Ro is hyperphosphorylated in the M phase. Phosphorylation did not change the recognition pattern of the anti-Ro sera.

En los pacientes que desarrollan lupus, su sistema inmune se activa y se vuelve contra el mismo huésped, por lo que es considerada una enfermedad autoinmune. En los Estados Unidos, existe más de un millón de personas que presenta Lupus. Sus síntomas aparecen en una gran variedad de formas, en los cuales la mitad de los casos es letal. El daño aparece en cualquier órgano del cuerpo y puede causar artritis con inflamación, fatiga, eritema en alas de mariposa en región malar, úlceras orales, fotosensibilidad, serositis (inflamación del tejido alrededor del corazón y pulmón), osteoporosis, desórdenes renales (proteinuria y destrucción celular), desórdenes sanguíneos (leucopenia, linfopenia, trombocitopenia, anemia hemolítica), desórdenes inmunológicos (anticuerpos anti-DNA y anti-Sm) y títulos de anticuerpos antinucleares anormales. Utilizando técnicas de biología molecular, se han descubierto algunos factores que regulan el sistema inmune, así como mecanismos bioquímicos por los cuales en el lupus se presenta daño al tejido. También se han identificado algunos genes candidato que parecen estar involucrados en el lupus.

PE and its severity are associated with the underexpression of placental MINA, and the G/G genotype of the MINA rs4857304 variant may modify the risk of severe PE among the PE cases evaluated.

El sistema inmune (SI) tiene como función primordial la defensa del organismo, a través del reconocimiento de antígenos potencialmente patógenos y su eliminación mediante dos mecanismos efectores: la inmunidad humoral y la inmunidad celular. Sin embargo, éstos pueden fallar por una inadecuada respuesta a patógenos (inmunodeficiencia), por falta de reconocimiento a lo propio (autoinmunidad) o por una respuesta exagerada e inapropiada a un antígeno (hipersensibilidad). Por tanto, el reconocimiento de lo propio y lo no propio por el sistema inmune es de capital importancia para el entendimiento de la autoinmunidad. Para prevenir la autoagresión, el SI cuenta con mecanismos que le permiten identificar a los antígenos derivados de la misma (alogénicos) o de otras especies (xenogénicos) y puede distingirlos de los propios (singénicos). Una característica común de las enfermedades autoinmunes es el rompimiento de la tolerancia a los antígenos propios y una de las consecuencias de esta disfunción inmune es la producción de autoanticuerpos que reaccionan contra una gran variedad de proteínas propias, que son blanco para la producción de autoanticuerpos.

Periodontal disease (PD) is a degenerative and progressive inflammatory disease induced by supragingival plaque bacteria, which affects the tooth supporting tissue such as periodontal ligament, cementum and alveolar bone. The host response to infection by periodontal bacteria may be related to a process of acute humoral response or cellular response. The expression of heat shock proteins (Hsp) and P53 is important in apoptosis, cell cycle control in cellular homeostasis and stress are overexpressed. The baseline of this study was to determine the expression of Hsp70, Hsp90 and P53 in the tissue of patients with chronic periodontal disease and gingivitis. The oral tissues were obtained by surgery, and quantified the amount of protein and characterized by SDS-PAGE, Western blot. To detect the expression of Hsp70, Hsp90 and p53 were using monoclonal antibodies. Hsp 70 detecction by RT-PCR were performed using Super ScriptTM One-Step and densitometric analysis. Results: There was an increase of Hsp70 and 90, and a slight increase in p53 levels. By PCR Hsp70 expression was increased in initial and progresive periodontitis and in a low level in advanced.