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              "es" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Esquema simplificado de la respuesta inmunol&#243;gica celular a la bacteria <span class="elsevierStyleItalic">M&#46; tuberculosis</span>&#46; Los signos &#40;&#43;&#41; y &#40;&#8211;&#41; indican la retroalimentaci&#243;n positiva o negativa inducida por cada una de las c&#233;lulas o citocinas en condiciones normales&#46; Los puntos negros &#40;&#9679;&#41; indican los principales sitios en los que el glatir&#225;mero acetato &#40;GA&#41; participa directamente y las flechas indican si induce un efecto de aumento o de disminuci&#243;n&#46; El GA afecta directamente a la activaci&#243;n de macr&#243;fagos&#44; inhibiendo la respuesta de linfocitos T-helper 1 &#40;Th1&#41; y reduciendo la concentraci&#243;n de interfer&#243;n &#40;IFN&#41;-&#947; circulante&#44; que es fundamental para la activaci&#243;n de estos &#250;ltimos&#46; Tambi&#233;n induce una menor producci&#243;n de interleucina &#40;IL&#41; 12&#44; que amplifica la respuesta de los Th1<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">2</span></a>&#46; La producci&#243;n de IL-10 se incrementa&#44; lo que inhibe directamente la activaci&#243;n de macr&#243;fagos y bloquea los efectos de las c&#233;lulas dendr&#237;ticas &#40;CD&#41; y la diferenciaci&#243;n de linfocitos T no expuestos en linfocitos Th1<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">4</span></a>&#46; Bloquea la migraci&#243;n de linfocitos Th1 desde los ganglios linf&#225;ticos hacia los pulmones&#44; e inhibe la expresi&#243;n y liberaci&#243;n de TNF-&#945;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">4</span></a>&#46; Finalmente&#44; el GA estimula a los linfocitos T-reguladores&#44; que tambi&#233;n bloquean la respuesta de los linfocitos Th1<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">4</span></a>&#46;</p>"
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          "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">A simplified scheme of the cellular immune response to <span class="elsevierStyleItalic">M&#46; tuberculosis</span>&#46; The &#40;&#43;&#41; and &#40;&#8722;&#41; signs indicate the positive or negative feedback induced by each cell or cytokine under normal circumstances&#46; The main sites where glatiramer acetate &#40;GA&#41; directly participates are marked with a black dot &#40;&#8226;&#41; and arrow to indicate the induced effect &#40;increase or decrease&#41;&#46; It directly affects macrophage activation &#40;M act&#41; by inhibiting T-helper 1 &#40;Th1&#41; response and thus&#44; reducing levels of circulating interferon &#40;IFN&#41; &#947;&#44; which plays an important role in their activation&#46; It inhibits production of interleukin &#40;IL&#41; 12 which amplifies the Th1 response&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">3</span></a> The IL-10 production is increased&#44; directly inhibiting macrophage activation&#44; and blocking the effects of dendritic cells &#40;DC&#41; and the differentiation of naive T cells into Th1 cells&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">4</span></a> It blocks the migration of Th1 cells from lymph nodes back to the lungs&#44; and inhibits the expression and release of tumor necrosis factor &#40;TNF&#41;-&#945;&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">4</span></a> Finally&#44; it stimulates T-regulatory &#40;T-reg&#41; cells which also block the Th1 response&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">4</span></a></p>"
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Glatiramer acetate &#40;GA&#41; is a synthetic copolymer-1 approved as first-line treatment for relapsing-remitting multiple sclerosis &#40;RRMS&#41;&#46; Several studies have indicated that GA modulates different levels of the immune response&#44; but no specific warnings regarding its use and potential reactivation of latent tuberculosis &#40;TB&#41; infection exist&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">1</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">A 37-year-old man&#44; engineer&#44; active smoker &#40;10 pack-years&#41;&#44; with a 6-year history of RRMS but otherwise healthy&#44; attended our pulmonary clinic reporting a 1-week history of productive cough&#44; fever&#44; left side pleuritic chest pain&#44; and malaise&#46; He had been taking daily subcutaneous GA since his RRMS diagnosis&#44; but no other concomitant medication&#46; Relevant past medical history included a 9-month course of isoniazid as primary chemoprophylaxis for TB 16 years previously&#44; after a positive tuberculin skin test as part of a TB contact study&#46; He denied any other subsequent known contacts or exposure to high-risk environments&#46; His physical exam was normal and blood tests showed a mild elevation of acute phase reactants&#46; A chest computed tomography revealed left upper lobe alveolar infiltrate and a 1&#46;8<span class="elsevierStyleHsp" style=""></span>cm lung cavity&#46; The sputum smear was positive for acid-fast bacilli and empiric 4-drug treatment was started&#46; Sputum culture confirmed <span class="elsevierStyleItalic">Mycobacterium tuberculosis</span> and the patient recovered completely after 6 months of treatment&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">Peripheral immunomodulatory mechanisms of GA include&#58; binding to major histocompatiblity class II molecules&#44; alteration of the innate immune response&#44; T-cell receptor antagonism&#44; T-cell deviation and modification of B-cells&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">1</span></a> It has an inhibitory effect on monocyte reactivity&#44; modifying dendritic cells and monocytes secretion to produce less tumor necrosis factor &#40;TNF&#41;-&#945; and interleukin &#40;IL&#41;-12&#44; and more IL-10 and transforming growth factor &#40;TGF&#41;-&#946;&#46; It stimulates T-helper &#40;Th&#41;-2 anti-inflammatory response&#44; in detriment of Th1 pro-inflammatory effects&#44; with subsequent decrease of interferon &#40;IFN&#41;-&#947; levels&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">The initial defense against TB infection involves alveolar macrophages&#46; Although there is a role for many types of T-lymphocytes&#44; the major effector cell in cell-mediated immunity in TB is the helper T-cell&#46; Studies have shown that patients with active TB have mainly a Th2-type response&#44; whereas those with latent disease show a Th1-type response&#46; The strength of the latter relates directly to the clinical manifestations of the disease&#44; where low levels of circulating IFN-&#947; in peripheral blood are associated with severe clinical TB and advanced disease&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">3</span></a> Inhibition of TNF-&#945; and reduced levels of IL-12&#44; both effects of GA treatment&#44; are associated with increased risk of mycobacterial disease&#46; GA also affects macrophage activation&#44; critical in the elimination of mycobacteria&#44; as increased levels of IL-10 and TGF-&#946; and reduced levels of IFN-&#947; are associated with macrophage inactivation and activation&#44; respectively&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">3</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall"><a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a> illustrates the different sites where GA would intervene in the immune response to <span class="elsevierStyleItalic">M&#46; tuberculosis</span>&#46; These effects are likely to induce an imbalance between the pro- and anti-inflammatory factors that control TB infection&#44; facilitating disease reactivation&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">2</span></a></p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0030" class="elsevierStylePara elsevierViewall">To the best of our knowledge this is the first documented case of pulmonary TB reactivation in a patient receiving GA treatment&#46; Screening for latent TB infection may be an important first step before starting GA in patients with RRMS&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Funding</span><p id="par0035" class="elsevierStylePara elsevierViewall">No funding was received&#46;</p></span></span>"
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          "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">A simplified scheme of the cellular immune response to <span class="elsevierStyleItalic">M&#46; tuberculosis</span>&#46; The &#40;&#43;&#41; and &#40;&#8722;&#41; signs indicate the positive or negative feedback induced by each cell or cytokine under normal circumstances&#46; The main sites where glatiramer acetate &#40;GA&#41; directly participates are marked with a black dot &#40;&#8226;&#41; and arrow to indicate the induced effect &#40;increase or decrease&#41;&#46; It directly affects macrophage activation &#40;M act&#41; by inhibiting T-helper 1 &#40;Th1&#41; response and thus&#44; reducing levels of circulating interferon &#40;IFN&#41; &#947;&#44; which plays an important role in their activation&#46; It inhibits production of interleukin &#40;IL&#41; 12 which amplifies the Th1 response&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">3</span></a> The IL-10 production is increased&#44; directly inhibiting macrophage activation&#44; and blocking the effects of dendritic cells &#40;DC&#41; and the differentiation of naive T cells into Th1 cells&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">4</span></a> It blocks the migration of Th1 cells from lymph nodes back to the lungs&#44; and inhibits the expression and release of tumor necrosis factor &#40;TNF&#41;-&#945;&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">4</span></a> Finally&#44; it stimulates T-regulatory &#40;T-reg&#41; cells which also block the Th1 response&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">4</span></a></p>"
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