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10.1111/j.1600-065x.1997.tb01010.x http://scihub22266oqcxt.onion/10.1111/j.1600-065x.1997.tb01010.x 9416506!ä!9416506 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 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Immunol+Rev 1997 ; 159 (ä): 105-17 Nephropedia Template TP {{tp|p=9416506|t=1997. Effector CD4+ and CD8+ T-cell mechanisms in the control of respiratory virus infections |pdf=|usr=}}{{9416506}} gab.com Text Effector CD4+ and CD8+ T-cell mechanisms in the control of respiratory virus infections JO: Immunol Rev http://www.kidney.de/pget.php?&tw=1&pmid=9416506 #FOAvip The rules for T-cell-mediated control of viruses that infect via the respiratory mucosae show both common themes and differences, depending on the nature of the pathogen. Virus-specific CD8+ cytotoxic T lymphocytes (CTLs) are the key effectors of virus clearance in mice infected with both negative strand RNA viruses (influenza and Sendai) and a DNA virus, the murine gamma-herpesvirus-68 (MHV-68). Recently completed experiments establish that these activated CD8+ T cells indeed operate primarily via contact-dependent lysis. Perforin-mediated cytotoxicity seems to be the preferred mode, though a Fas-based mechanism can apparently serve as an alternative mechanism. Immune CD4+ T cells functioning in the absence of the CD8+ subset cannot eliminate MHV-68 from lung epithelial cells, are somewhat less efficient than the CD8+ CTLs at clearing the RNA viruses, and are generally ineffectual in mice that lack B lymphocytes. Though cytokine secretion by CD4+ and CD8+ T cells in the virus-infected lung may promote both T-cell extravasation and macrophage activation, such processes are not alone sufficient to deal consistently with any of these infections. However, CD4+ T help is mandatory for an effective B-cell response, and can operate to promote the clonal expansion of virus-specific CD8+ T cells in the lymph nodes and spleen. Furthermore, a concurrent CD4+ T-cell response seems to be essential for maintaining continued CD8+ T-cell surveillance and effector capacity through the persistent, latent phase of MHV-68 infection in B cells. Thus, the evidence to date supports a very traditional view; CD8+ T cells function mainly as killers and the CD4+ T cells as helpers in these respiratory virus infections. Twit Text FOAVip Effector CD4+ and CD8+ T-cell mechanisms in the control of respiratory virus infections ????Immunol Rev http://www.kidney.de/pget.php?&tw=1&pmid=9416506 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=9416506 #FOAvip English Wikipedia <ref>{{Cite pmid|9416506}}</ref> Effector CD4+ and CD8+ T-cell mechanisms in the control of respiratory virus infections #MMPMID9416506 Doherty PC; Topham DJ; Tripp RA; Cardin RD; Brooks JW; Stevenson PG Immunol Rev 1997[Oct]; 159 (ä): 105-17 PMID9416506show ga The rules for T-cell-mediated control of viruses that infect via the respiratory mucosae show both common themes and differences, depending on the nature of the pathogen. Virus-specific CD8+ cytotoxic T lymphocytes (CTLs) are the key effectors of virus clearance in mice infected with both negative strand RNA viruses (influenza and Sendai) and a DNA virus, the murine gamma-herpesvirus-68 (MHV-68). Recently completed experiments establish that these activated CD8+ T cells indeed operate primarily via contact-dependent lysis. Perforin-mediated cytotoxicity seems to be the preferred mode, though a Fas-based mechanism can apparently serve as an alternative mechanism. Immune CD4+ T cells functioning in the absence of the CD8+ subset cannot eliminate MHV-68 from lung epithelial cells, are somewhat less efficient than the CD8+ CTLs at clearing the RNA viruses, and are generally ineffectual in mice that lack B lymphocytes. Though cytokine secretion by CD4+ and CD8+ T cells in the virus-infected lung may promote both T-cell extravasation and macrophage activation, such processes are not alone sufficient to deal consistently with any of these infections. However, CD4+ T help is mandatory for an effective B-cell response, and can operate to promote the clonal expansion of virus-specific CD8+ T cells in the lymph nodes and spleen. Furthermore, a concurrent CD4+ T-cell response seems to be essential for maintaining continued CD8+ T-cell surveillance and effector capacity through the persistent, latent phase of MHV-68 infection in B cells. Thus, the evidence to date supports a very traditional view; CD8+ T cells function mainly as killers and the CD4+ T cells as helpers in these respiratory virus infections. |Animals[MESH] |B-Lymphocytes/immunology[MESH] |CD4-Positive T-Lymphocytes/*immunology[MESH] |CD8-Positive T-Lymphocytes/*immunology[MESH] |Cytotoxicity, Immunologic[MESH] |Mice[MESH] |Pneumonia, Viral/*immunology[MESH]Effector CD4+ and CD8+ T-cell mechanisms in the control of respiratory(epmc).pdf DeepDyve Pubget Overpricing