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However, side effects hinder\n                      <jats:styled-content style=\"fixed-case\">PDE<\/jats:styled-content>\n                      4 inhibitors clinical use.\n                      <jats:styled-content style=\"fixed-case\">PDE<\/jats:styled-content>\n                      7 inhibition might constitute an alternative therapeutic strategy, but few data about the anti\u2010inflammatory potential of\n                      <jats:styled-content style=\"fixed-case\">PDE<\/jats:styled-content>\n                      7 inhibitors are currently available. We have used the\n                      <jats:styled-content style=\"fixed-case\">EAE<\/jats:styled-content>\n                      model to perform a comparative evaluation of\n                      <jats:styled-content style=\"fixed-case\">PDE<\/jats:styled-content>\n                      4 and\n                      <jats:styled-content style=\"fixed-case\">PDE<\/jats:styled-content>\n                      7 inhibition as strategies for\n                      <jats:styled-content style=\"fixed-case\">MS<\/jats:styled-content>\n                      treatment.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental Approach<\/jats:title>\n                    <jats:p>\n                      Two\n                      <jats:styled-content style=\"fixed-case\">PDE<\/jats:styled-content>\n                      7 inhibitors, the sulfonamide derivative\n                      <jats:styled-content style=\"fixed-case\">BRL<\/jats:styled-content>\n                      50481 and the recently described quinazoline compound\n                      <jats:styled-content style=\"fixed-case\">TC<\/jats:styled-content>\n                      3.6, were assayed to modulate\n                      <jats:styled-content style=\"fixed-case\">EAE<\/jats:styled-content>\n                      in\n                      <jats:styled-content style=\"fixed-case\">SJL<\/jats:styled-content>\n                      mice, in comparison with the well\u2010known\n                      <jats:styled-content style=\"fixed-case\">PDE<\/jats:styled-content>\n                      4 inhibitor Rolipram. We evaluated clinical signs, presence of inflammatory infiltrates in\n                      <jats:styled-content style=\"fixed-case\">CNS<\/jats:styled-content>\n                      and anti\u2010inflammatory markers. We also analysed the effect of these inhibitors on the inflammatory profile of spleen cells\n                      <jats:italic>in vitro<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Results<\/jats:title>\n                    <jats:p>\n                      <jats:styled-content style=\"fixed-case\">TC<\/jats:styled-content>\n                      3.6 prevented\n                      <jats:styled-content style=\"fixed-case\">EAE<\/jats:styled-content>\n                      with efficacy similar to Rolipram, while\n                      <jats:styled-content style=\"fixed-case\">BRL<\/jats:styled-content>\n                      50481 had no effect on the disease. Differences between both\n                      <jats:styled-content style=\"fixed-case\">PDE<\/jats:styled-content>\n                      7 inhibitors are discussed. Data from Rolipram and\n                      <jats:styled-content style=\"fixed-case\">TC<\/jats:styled-content>\n                      3.6 showed that\n                      <jats:styled-content style=\"fixed-case\">PDE<\/jats:styled-content>\n                      4 and\n                      <jats:styled-content style=\"fixed-case\">PDE<\/jats:styled-content>\n                      7 inhibition work through both common and distinct pathways. Rolipram administration caused an increase in\n                      <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                      \u201010 and\n                      <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                      \u201027 expression which was not found after\n                      <jats:styled-content style=\"fixed-case\">TC<\/jats:styled-content>\n                      3.6 treatment. On the other hand, both inhibitors reduced\n                      <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                      \u201017 levels, prevented infiltration in\n                      <jats:styled-content style=\"fixed-case\">CNS<\/jats:styled-content>\n                      and increased the expression of the\n                      <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\n                      regulator cell marker\n                      <jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>\n                      oxp3.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions and Implications<\/jats:title>\n                    <jats:p>\n                      These results provide new information about the effects of Rolipram on\n                      <jats:styled-content style=\"fixed-case\">EAE<\/jats:styled-content>\n                      , underline\n                      <jats:styled-content style=\"fixed-case\">PDE<\/jats:styled-content>\n                      7 inhibition as a new therapeutic target for inflammatory diseases and show the value of\n                      <jats:styled-content style=\"fixed-case\">TC<\/jats:styled-content>\n                      3.6 to prevent\n                      <jats:styled-content style=\"fixed-case\">EAE<\/jats:styled-content>\n                      , with possible consequences for new therapeutic tools in\n                      <jats:styled-content style=\"fixed-case\">MS<\/jats:styled-content>\n                      .\n                    <\/jats:p>\n                  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