Anti-Mi-2 antibodies.

Autoantibodies targeting the Mi-2 nuclear antigen represent one of the serologic hallmarks of idiopathic inflammatory myopathies, with a diagnostic sensitivity and specificity of approximately 4-18% and 98-100%, respectively. Mi-2 antigen is a component of the nuclesome remodeling-deacetylase (NuRD) complex involved in transcription regulation.Anti-Mi-2 antibodies are strongly associated with dermatomyositis (frequency up to 31%) and have a very high positive predictive value for such disease subset. A strong correlation with HLA-DR7 has been demonstrated. At the moment, optimal serologic testing is achieved by ELISA screening on recombinant Mi-2 antigen and confirmation of positive results on immunoblot.

Anti-Jo-1 antibodies.

Anti-Jo-1 antibody is a myositis specific autoantibody most commonly found in patients with idiopathic inflammatory myopathies (IIM). This antibody is directed against the histidyl-tRNA synthetase which catalyses the binding of the histidine to its cognate tRNA during protein synthesis. It can be considered a specific marker of IIM, predominantly found in 20-30% of patients with PM and in the 60-70% of those with interstitial pulmonary fibrosis. These antibodies are also found in DM, although less frequently than in PM, and are rare in children with PM or DM and in other connective tissue diseases.ELISA, CIE and immunoblotting are highly specific and sensitive techniques for testing anti-Jo-1 antibodies. The detection of this antibody is particularly useful in diagnosis and classification of IIM. Moreover, anti-Jo-1 serum levels strongly correlate with disease activity representing a good marker for disease monitoring.

Pregnancy, cytokines, and disease activity in systemic lupus erythematosus.

OBJECTIVE: To evaluate levels of selected cytokines and soluble receptors involved in the humoral immune response during pregnancy in systemic lupus erythematosus (SLE) patients. METHODS: Seventeen consecutive SLE patients and 8 matched healthy controls were prospectively studied during pregnancy. Sera were obtained within the last 3 months prior to pregnancy; at 9, 17, and 29 weeks of pregnancy; and at 1 month after delivery. Serum levels of interleukin-10 (IL-10), interleukin-6 (IL-6), and soluble tumor necrosis factor receptors p55 (sTNFR I) and p75 (sTNFR II) were evaluated. SLE activity was measured by the European Consensus Lupus Activity Measurement score modified for pregnancy. RESULTS: IL-10 serum levels were found to be higher (P <0.0001) in patients than in controls before conception, and still higher (P <0.0001) in SLE patients during gestation, without intertrimester changes. In SLE patients, IL-6 serum levels did not increase in the third trimester of pregnancy, as was observed in controls (P=0.011). No significant differences between SLE patients and controls were found in either sTNFR I or II levels or profiles before and during pregnancy. IL-10 and sTNFR I levels were significantly higher during pregnancy and postpartum in SLE patients with active disease (P=0.03 and P=0.01, respectively). CONCLUSION: The levels of some cytokines involved in the humoral immune response seem to be modified in the peripheral circulation of pregnant SLE patients. The most relevant modifications are the lower than expected increase of IL-6 in the third trimester of gestation and persistently high levels of IL-10 during pregnancy.

Steroid hormones and disease activity during pregnancy in systemic lupus erythematosus.

OBJECTIVES: To analyze the variation of steroid hormone levels during pregnancy in patients with systemic lupus erythematosus (SLE). Moreover, to investigate whether, during gestation, there is any relationship between steroid concentration and SLE activity. METHODS: Seventeen consecutive pregnant SLE patients and 8 matched healthy pregnant controls were studied prospectively. Disease activity was evaluated by European Consensus Lupus Activity Measure (ECLAM) score modified for pregnancy. The following hormones were evaluated: testosterone, 17beta-estradiol (estradiol), cortisol, dehydroepiandrosterone sulfate (DHEAS), and progesterone. RESULTS: Disease activity score significantly varied during pregnancy and postpartum (P< 0.05), being decreased in the third trimester and increased in the second trimester and postpartum. Serum levels of all steroids varied significantly during pregnancy and the postpartum period both in patients and in healthy subjects. In SLE patients, estradiol, progesterone, and DHEAS concentrations were found to be significantly reduced compared with controls. Serum level profiles of estradiol and progesterone were different from those observed in controls. No differences in the steroid levels were observed between patients taking prednisone 5 mg/day, apart from cortisol, which was, as expected, lower in the latter group. CONCLUSIONS: The major hormonal alteration observed during pregnancy in SLE patients was an unexpected lack of estrogen serum level increase, and, to a lesser extent, progesterone serum level increase, during the second and-even more-the third trimester of gestation. This lack of increase probably was due to placental compromise. Therefore, these steroid hormone variations may result in a lower humoral immune response activation, probably related to a change in the estrogen/androgen balance, that in turn could account for the decrease in disease activity observed during the third trimester in pregnant SLE patients.