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| 1 | IL-17 in systemic lupus erythematosu显示文摘 | Crispín JC Tsokos GC | 2010 | J Biomed Biotechnol2010，，： | 1 |
| 2 | Quantitative and qualitative normal regulatory T cells are not capable of inducing suppression in SLE patients due to T-cell resistance显示文摘 | Vargas-Rojas MI Crispín JC Richaud-Patin Y | | 0，，04： | 1 |
| 3 | How signaling and gene transcription aberrations dictate the systemic lupus erythematosus T cell phenotype显示文摘 | Crispín JC Kyttaris VC Juang YT | | 0，，03： | 1 |
| 4 | Novel molecular targets in the treatment of systemic lupus erythematosus显示文摘 | Crispín JC Tsokos GC | | 0，，03： | 1 |
| 5 | Transcriptional regulation of IL-2 in health and autoimmunity显示文摘 | José C. Crispín George C. Tsokos | 2008 | Autoimmunity Reviews2008，，3： | 1 |
| 6 | IL-17 producing CD4+T cells mediate accelerated ischemia/reperfusion-induced injury in autoimmunity-prone mice显示文摘 | Edgerton C Crispín J C Moratz C M | 2009 | Clin Immunol2009，130，： | 1 |
| 7 | Pathogenesis of human systemic lupus erythematosus:recent advances显示文摘 | Crispín JC Liossis SN Kis-Toth K | 2010 | Trends Mol Med2010，16，2： | 1 |
| 8 | Systemic lupus erythematosus:new molecular targets显示文摘 | Crispín J C Kyttaris V Juang Y T | 2007 | Ann Rheum Dis2007，66，9： | 1 |
| 9 | T cells as therapeutic targets in SLE显示文摘 | Crispín JC Kyttaris VC Terhorst C | 2010 | Nat Rev Rheumatol2010，6，： | 1 |
| 10 | Pathogenesis of human systemic lupus erythematosus:recent advances显示文摘 | Crispín JC Liossis SN Kis-Toth K | 2010 | Trends Mol Med2010，16，： | 1 |
| 11 | Adult-onset Still disease as the cause of fever of unknown origin显示文摘 | Crispín J C Martínez-Baos D Alcocer-Varela J | 2005 | Medicine(Baltimore)2005，84，6： | 1 |
| 12 | IL-17-producing T cells in lupus nephritis显示文摘 | Apostolidis SA Crispín JC Tsokos GC | 2011 | Lupus2011，20，2： | 1 |
| 13 | A novel inhibitor of the alternative pathway of complement attenuates intestinal ischemia/reperfusion-induced injury显示文摘 | Chen J Crispín JC Dalle Lucca J | 2011 | J Surg Res2011，167，2： | 1 |
| 14 | Adult-onset Still disease as the cause of fever of unknown origin显示文摘 | Crispín JC Martínez-Baos D Alcocer-Varela J | 2005 | Medicine(Baltimore)2005，84，6： | 1 |
| 15 | Pathogenesis of human systemic lupus erythematosus:recent advances显示文摘 | Crispín JC Liossis SNC Kis-Toth K | 2010 | Trends Mo Med2010，16，2： | 1 |
| 16 | Interleukin-17 and systemic lupus erythematosus:current concepts显示文摘 | Nalbandian A Crispín JC Tsokos GC | 2009 | Clin Exp Immunol2009，157，2： | 1 |
| 17 | IL-17-producing T cells in lupus nephritis显示文摘 | Apostolidis SA Crispín JC Tsokos GC | 2011 | Lupus2011，20，2： | 1 |
| 18 | Lessons from Sj?gren's syndrome etiopathogenesis:Novel cellular and molecular targets显示文摘Sj?gren's syndrome(SS) is a systemic autoimmune disease that affects primarily the lacrimal and salivary glands. In addition to a systemic autoimmune response directed against ubiquitous antigens(such as Ro and La antigens),patients with SS mount a localized response that affects the epithelial component of exocrine glands leading to the establishment of a destructive inflammatory infiltrate comprised of activated T and B cells. Local chemokine and cytokine production drive the recruitment and local activation of immune cells that cause injury to acinar cells. CD4 T cells with different functional differentiation programs including Th1(IFN-γ),Th2(IL-13,IL-4) and Th17(IL-17,IL-21,IL-22) as well as diverse cytokine signaling pathways,are involved at the initiation,perpetuation,and progression of the disease. Which factors initiate this response and allow it to become chronic are unknown. Proposed mechanisms include viral infections and acinar cell apoptosis. Moreover risk-conferring genetic variants,probably through the facilitation of innate and adaptive immune activation,most certainly contribute to the creation of an underlying environment that fosters tolerance loss and facilitates perpetuation of the autoimmune response. In this review,we describe the mechanisms through which the immune response causes SS and emphasize the pathways that are amenable of being targeted with therapeutic purposes. | José C Crispín Florencia Rosetti Gabriela Hernández-Molina | 2015 | World Journal of Immunology2015，5，3： | 0 |
| 19 | CaMK4-dependent activation of AKT/mTOR and CREM-[alpha] underlies autoimmunity-associated Th17 imbalance显示文摘 | Koga Tomohiro Hedrich Christian M Mizui Masayuki Yoshida Nobuya Otomo Kotaro Lieberman Linda A Rauen Thomas Crispín José C Tsokos George C | 2014 | Journal of Clinical Investigation2014，，5： | 1 |
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