Background mTOR inhibitor therapy is solely monitored via pharmacokinetics after kidney transplantation, which may not accurately reflect the effectiveness of PI3K-Akt-mTOR pathway blockade, potentially leading to inadequate or excessive immunosuppression. The pharmacodynamic effect of mTOR inhibition on NK cells and ...

Introduction T regulatory (Treg) cells play a crucial role in immune system homeostasis and in the pathogenesis of immune-mediated inflammatory diseases. Accordingly, numerous studies have examined the number and function of these lymphocytes in patients with different conditions as well as in healthy controls. The aim of ...

Potent inflammatory responses stemming from innate and T cell activation are initiated during acute human immunodeficiency virus (HIV) infection. Suppression of the virus replication by antiretroviral therapy reduces but does not normalize immune activation. By now, it is clear that residual immune activation can persist ...

Chronic prostatitis and chronic pelvic pain syndrome (CP/CPPS) are diagnosed in patients with various pelvic or genitourinary symptoms irrespective of the presence of a tender prostate. The etiology of chronic nonbacterial prostatitis remains unclear. Current treatments such as alpha-blockers, neuroleptics, ...

Introduction Deficiency of X-linked inhibitor of apoptosis protein (XIAP) is an X-linked recessive inborn error of immunity characterized by abnormal immune responses leading to inflammatory bowel disease and hemophagocytic lymphohistiocytosis. Although XIAP protein expression analysis by flow cytometry (XIAP flow) is ...

In this work we described a standardized method based on the development and validation of a synthetic control to solve the problem of test comparison. Inter-assay and inter-laboratory variability were assessed by multiple repeated analyses within the same laboratory, and between two different laboratories involved in the study. The method has been validated by evaluating the IFN signature of 39 patients with inflammatory disorders known to be related or not to Type I IFN (i.e. monogenic interferonopathies, systemic lupus erythematosus, juvenile dermatomyositis, periodic fevers, juvenile idiopathic arthritis).