This effect will depend probably on the properties of B cell-depleting agents and the susceptibility of autoreactive B cell clones Selleck KU-60019 to the
immunomodulatory activities of these agents. Equally important is the timing of the administration of B cell-depleting agents, whereby it can deplete the pool of autoreactive B cells early enough before these cells develop into plasma or memory B cells which are capable of producing high levels of pathogenic autoantibodies of IgG classes that can cross the placental barrier in sufficient quantities to reach a threshold that can cause damage to the fetal tissues. Such effects may have a novel clinical application Decitabine supplier in preventing life-threatening conditions such as NFAIT or congenital malformations such as congenital heart block, a long-term condition that is currently unpreventable.
The development of new B cell-targeted therapies may also improve the specificity of depletion of autoreactive B cells while sparing the beneficial regulatory B cell subsets and the protective natural antibody responses to maximize the benefits and minimize the risks of sustained suppression of the B cell compartment [116-118]. Therefore, lessons from future clinical studies and new developments in B cell-targeted therapies are important and necessary to give the newborn of a high-risk pregnancy a better chance at a healthy start to life. Our literature review was performed by searching in MEDLINE and PubMed database using search terms ‘Autoimmune’, ‘B cell’, ‘B-cell depletion’, ‘Pregnancy’ and ‘Rituximab’. All included articles were in English-language, full-text papers published
between 1975 and May 2012. We also searched reference list of these Cytidine deaminase articles. The authors thank Dr Christopher Jackson for their critical reading of this manuscript. J.M.M. and C.W.W. are funded by the Australian National Health and Medical Research Council. The authors declare no conflicts of interest. “
“A prevalent T helper type 1 (Th1) subset of lymphocytes has been described in Hashimoto’s thyroiditis (HT), but whether a similar polarization may characterize HT when associated with non-endocrine autoimmune disorders (NEAD) is not known. The aim of the present study was to analyse the intracellular Th1 and Th2 distinctive cytokines in patients with isolated HT or associated with non-endocrine autoimmune disorders. Intracellular cytokine expression was assessed in peripheral blood lymphocytes (PBL) of 68 out-patients (females = 55; males = 13; median age = 36 years) with HT : 33 had isolated HT and 35 had a concurrent NEAD.
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