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10.3389/fvets.2014.00020 http://scihub22266oqcxt.onion/10.3389/fvets.2014.00020 C4668878!4668878!26664919     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Front+Vet+Sci 2014 ; 1 (ä): ä Nephropedia Template TP {{tp|p=26664919|t=2014. Regulatory T Cell Activity and Signs of T Cell Unresponsiveness in Bovine Paratuberculosis |pdf=|usr=}}{{26664919}} gab.com Text Regulatory T Cell Activity and Signs of T Cell Unresponsiveness in Bovine Paratuberculosis JO: Front Vet Sci http://www.kidney.de/pget.php?&tw=1&pmid=26664919 #FOAvip Johne?s disease, caused by infection with Mycobacterium avium subspecies paratuberculosis (MAP), is a wasting disease of ruminants displaying a long subclinical stage of infection followed by clinical disease characterized by severe diarrhea, wasting, and premature death. Immunologically, subclinical disease is characterized by a Th1 response effective at controlling intracellular infections such as that caused by MAP. In late subclinical disease, the Th1 response subsides and a non-protective Th2 response becomes prominent. One hypothesis for this shift in immune paradigm is that a population of MAP-reactive regulatory T cells (Tregs) develops during subclinical infection, limiting Th1-type responses to MAP antigens. To investigate this, we sought to accomplish the following: (1) determine if CD4+CD25? T cells exposed to MAP-infected macrophages develop a Treg phenotype, (2) develop a method to expand the relative abundance of Tregs in bovine peripheral blood lymphocyte populations, and (3) identify functional activities of expanded Tregs when combined with autologous peripheral blood mononuclear cells (PBMCs) and live MAP. We found that CD4+CD25? T cells exposed to MAP-infected macrophages from cows with Johne?s disease do not show signs of a Treg phenotype and appear unresponsive to MAP antigens. A method for Treg expansion was successfully developed; however, based on results obtained in the subsequent functional studies it appears that these Tregs are not MAP-specific. Overall, it seems that T cell unresponsiveness, rather than Treg activity, is driving the Th1-to-Th2 immune shift observed during Johne?s disease. Further, we have successfully developed a method to enrich non-specific bovine Tregs that exert suppressive effects against Th1 cytokine production. Twit Text FOAVip Regulatory T Cell Activity and Signs of T Cell Unresponsiveness in Bovine Paratuberculosis ????Front Vet Sci http://www.kidney.de/pget.php?&tw=1&pmid=26664919 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26664919 #FOAvip English Wikipedia <ref>{{Cite pmid|26664919}}</ref> Regulatory T Cell Activity and Signs of T Cell Unresponsiveness in Bovine Paratuberculosis #MMPMID26664919 Roussey JA; Steibel JP; Coussens PM Front Vet Sci 2014[]; 1 (ä): ä PMID26664919show ga Johne?s disease, caused by infection with Mycobacterium avium subspecies paratuberculosis (MAP), is a wasting disease of ruminants displaying a long subclinical stage of infection followed by clinical disease characterized by severe diarrhea, wasting, and premature death. Immunologically, subclinical disease is characterized by a Th1 response effective at controlling intracellular infections such as that caused by MAP. In late subclinical disease, the Th1 response subsides and a non-protective Th2 response becomes prominent. One hypothesis for this shift in immune paradigm is that a population of MAP-reactive regulatory T cells (Tregs) develops during subclinical infection, limiting Th1-type responses to MAP antigens. To investigate this, we sought to accomplish the following: (1) determine if CD4+CD25? T cells exposed to MAP-infected macrophages develop a Treg phenotype, (2) develop a method to expand the relative abundance of Tregs in bovine peripheral blood lymphocyte populations, and (3) identify functional activities of expanded Tregs when combined with autologous peripheral blood mononuclear cells (PBMCs) and live MAP. We found that CD4+CD25? T cells exposed to MAP-infected macrophages from cows with Johne?s disease do not show signs of a Treg phenotype and appear unresponsive to MAP antigens. A method for Treg expansion was successfully developed; however, based on results obtained in the subsequent functional studies it appears that these Tregs are not MAP-specific. Overall, it seems that T cell unresponsiveness, rather than Treg activity, is driving the Th1-to-Th2 immune shift observed during Johne?s disease. Further, we have successfully developed a method to enrich non-specific bovine Tregs that exert suppressive effects against Th1 cytokine production. äRegulatory T Cell Activity and Signs of T Cell Unresponsiveness in Bov(epmc).pdf DeepDyve Pubget Overpricing