http://precedings.nature.com/tags/immunity Recently posted documents tagged with 'immunity' Nature Publishing Group en Nature Precedings http://precedings.nature.com/images/header_logo.gif http://precedings.nature.com http://precedings.nature.com/documents/2826/version/1 Interleukin (IL) -1, a proinflammatory cytokine, increases in aneurysm, and the IL-1 receptor antagonist (IL-1Ra) modulates IL-1 activity endogenously. We show here that IL-1Ra-deficiency in hematopoietic cells disrupts immune system homeostasis and causes spontaneous femoral artery aneurysms in mice lacking interventions such as drugs or surgery. Thus, IL-1Ra-deficient mice provide easy observations with age and diminish mortality that typically follows surgical procedures. Furthermore, since IL-1Ra-deficient mice contain the entire spectrum of lesions observed during inflammatory aneurysm, this mouse model likely will provide numerous opportunities to study the pathogenesis and therapy of inflammatory aneurysm. http://precedings.nature.com/documents/2826/version/1 Thu, 29 Jan 2009 10:41:53 UTC Deficiency of interleukin-1 receptor antagonist causes spontaneous femoral artery aneurysms hdl:10101/npre.2009.2826.1 2009-01-29 Kikuo Isoda Nature Precedings 2009-01-29T10:41:53Z Manuscript Molecular Cell Biology http://creativecommons.org/licenses/by/3.0/ http://precedings.nature.com/documents/2005/version/1 Current thinking emphasizes the primacy of CD14 in facilitating TLR recognition of microbes to initiate proinflammatory signaling events and the importance of p38-MAPK in augmenting such responses. Herein, this paradigm is challenged by demonstrating that recognition of Borrelia burgdorferi not only triggers an inflammatory response in the absence of CD14, but one that is uncontrolled as a consequence of impaired PI3K/AKT/p38-MAPK signaling and negative regulation of TLR2. CD14 deficiency results in hyperphosphorylation of AKT and reduced activation of p38. Such aberrant signaling leads to decreased negative regulation by SOCS1, SOCS3, and CIS thereby engendering a more severe and persistent inflammatory response to B. burgdorferi. Perturbation of this CD14/p38-MAPK-dependent mechanism of immune regulation may underlie development of infectious chronic inflammatory syndromes. http://precedings.nature.com/documents/2005/version/1 Wed, 25 Jun 2008 10:07:23 UTC CD14 Modulates PI3K/AKT/p38-MAPK Licensing of Negative Regulators of TLR Signaling to Restrain Chronic Inflammation hdl:10101/npre.2008.2005.1 2008-07-01 Timothy J. Sellati Nature Precedings 2008-06-25T10:07:23Z Manuscript Immunology Microbiology http://creativecommons.org/licenses/by/3.0/