<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Piscianz, Elisa</style></author><author><style face="normal" font="default" size="100%">Valencic, Erica</style></author><author><style face="normal" font="default" size="100%">Cuzzoni, Eva</style></author><author><style face="normal" font="default" size="100%">De Iudicibus, Sara</style></author><author><style face="normal" font="default" size="100%">De Lorenzo, Elisa</style></author><author><style face="normal" font="default" size="100%">Decorti, Giuliana</style></author><author><style face="normal" font="default" size="100%">Tommasini, Alberto</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Fate of lymphocytes after withdrawal of tofacitinib treatment.</style></title><secondary-title><style face="normal" font="default" size="100%">PLoS One</style></secondary-title><alt-title><style face="normal" font="default" size="100%">PLoS ONE</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Antigens, CD</style></keyword><keyword><style  face="normal" font="default" size="100%">B-Lymphocytes</style></keyword><keyword><style  face="normal" font="default" size="100%">CD4-Positive T-Lymphocytes</style></keyword><keyword><style  face="normal" font="default" size="100%">CD8-Positive T-Lymphocytes</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Proliferation</style></keyword><keyword><style  face="normal" font="default" size="100%">Drug Administration Schedule</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Janus Kinase 3</style></keyword><keyword><style  face="normal" font="default" size="100%">Killer Cells, Natural</style></keyword><keyword><style  face="normal" font="default" size="100%">Lymphocyte Activation</style></keyword><keyword><style  face="normal" font="default" size="100%">Lymphocyte Count</style></keyword><keyword><style  face="normal" font="default" size="100%">Phytohemagglutinins</style></keyword><keyword><style  face="normal" font="default" size="100%">Piperidines</style></keyword><keyword><style  face="normal" font="default" size="100%">Primary Cell Culture</style></keyword><keyword><style  face="normal" font="default" size="100%">Protein Kinase Inhibitors</style></keyword><keyword><style  face="normal" font="default" size="100%">Pyrimidines</style></keyword><keyword><style  face="normal" font="default" size="100%">Pyrroles</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">9</style></volume><pages><style face="normal" font="default" size="100%">e85463</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Tofacitinib (Tofa) is an inhibitor of Janus Kinase 3, developed for the treatment of autoimmune diseases and for the prevention of transplant rejection. Due to its selective action on proliferating cells, Tofa can offer a way to block T cell activation, without toxic effects on resting cells. However, few studies have investigated the effects of Tofa on lymphocyte activation in vitro. Our aim was to study the action of Tofa on different lymphocyte subsets after in vitro stimulation and to track the behaviour of treated cells after interruption of the treatment. Peripheral blood lymphocytes were stimulated in vitro with mitogen and treated with two concentrations of Tofa. After a first period in culture, cells were washed and further incubated for an additional time. Lymphocyte subsets, activation phenotype and proliferation were assessed at the different time frames. As expected, Tofa was able to reduce the activation and proliferation of lymphocytes in the first four days of treatment. In addition the drug led to a relative decrease of Natural Killer, B cells and CD8 T cells compared to CD4 T cells. However, treated cells were still viable after the first period in culture and begun to proliferate, strikingly, in a dose dependent manner when the drug was removed from the environment by replacing the culture medium. This novel data does not necessarily predict a similar behaviour in vivo, but can warn about the clinical use of this drug when a discontinuation of treatment with Tofa is considered for any reason.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/24416411?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Taddio, Andrea</style></author><author><style face="normal" font="default" size="100%">Biondi, Andrea</style></author><author><style face="normal" font="default" size="100%">Piscianz, Elisa</style></author><author><style face="normal" font="default" size="100%">Valencic, Erica</style></author><author><style face="normal" font="default" size="100%">Biagi, Ettore</style></author><author><style face="normal" font="default" size="100%">Badolato, Raffaele</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">From bone marrow transplantation to cellular therapies: possible therapeutic strategies in managing autoimmune disorders.</style></title><secondary-title><style face="normal" font="default" size="100%">Curr Pharm Des</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Curr. Pharm. Des.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Autoimmune Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Bone Marrow Transplantation</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Chronic Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Graft vs Host Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Hematopoietic Stem Cell Transplantation</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammation</style></keyword><keyword><style  face="normal" font="default" size="100%">Lymphocytes</style></keyword><keyword><style  face="normal" font="default" size="100%">Mesenchymal Stem Cell Transplantation</style></keyword><keyword><style  face="normal" font="default" size="100%">T-Lymphocytes, Regulatory</style></keyword><keyword><style  face="normal" font="default" size="100%">Treatment Outcome</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">18</style></volume><pages><style face="normal" font="default" size="100%">5776-81</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Chronic inflammatory disorders occurring in childhood represent a serious therapeutic challenge. However, available therapies seem not to be targeted on the pathogenic mechanism of the disease and are often not actively affecting the natural history of the disease. Emerging treatments might be of some benefit to many patients who did not respond to conventional therapeutic options. Biological therapies with monoclonal antibodies and other recombinant proteins have been introduced in clinical practice. At the same time, mesenchymal stromal cells (MSC) have gained attention as a savage treatment in patients subjected to hematopoietic stem cell transplantation who develop severe graft versus host disease (GvHD); in addition, recent reports from clinical trials on larger cohorts of patients support their use as second-line treatment after failure of corticosteroid treatment. For analogy, they have been proposed for the treatment of intractable autoimmune disorders. Hematopoietic stem cell transplantation (HSCT) has been shown to be effective for treatment of rheumatic disorder cases that were resistant to traditional therapies especially if combined with cell manipulation techniques, such as selection of regulatory T cell and depletion of harmful lymphocytes. We herein present the rationale of different strategies, the preliminary data obtained in clinical trials, unsolved problems and possible next developments of novel treatment protocols of autoimmune disorders.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">35</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22726117?dopt=Abstract</style></custom1></record></records></xml>