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Bone Marrow Stromal Cells Use Tgf-Β To Suppress Allergic Responses In A Mouse Model Of Ragweed-Induced Asthma, K. Nemeth, A. Keane-Myers, J. M. Brown, D. D. Metcalfe, J. D. Gorham
Bone Marrow Stromal Cells Use Tgf-Β To Suppress Allergic Responses In A Mouse Model Of Ragweed-Induced Asthma, K. Nemeth, A. Keane-Myers, J. M. Brown, D. D. Metcalfe, J. D. Gorham
Dartmouth Scholarship
Bone marrow stromal cells [BMSCs; also known as mesenchymal stem cells (MSCs)] effectively suppress inflammatory responses in acute graft-versus-host disease in humans and in a number of disease models in mice. Many of the studies concluded that BMSC- driven immunomodulation is mediated by the suppression of pro- inflammatory Th1 responses while rebalancing the Th1/Th2 ratio toward Th2. In this study, using a ragweed induced mouse asthma model, we studied if BMSCs could be beneficial in an allergic, Th2- dominant environment. When BMSCs were injected i.v. at the time of the antigen challenge, they protected the animals from the majority of …
Deficient Cd40-Traf6 Signaling In Leukocytes Prevents Atherosclerosis By Skewing The Immune Response Toward An Antiinflammatory Profile, Esther Lutgens, Dirk Lievens, Linda Beckers, Erwin Wijnands, Oliver Soehnlein, Alma Zernecke, Tom Seijkens, David Engel, Jack Cleutjens, Anna M. Keller, Shalin H. Naike, Louis Boon, Hafid Ait Oufella, Ziad Mallat, Cory L. Ahonen, Randolph J. Noelle, Menno P. De Winther, Mat J. Daemen, Erik A. Biessen, Christian Weber
Deficient Cd40-Traf6 Signaling In Leukocytes Prevents Atherosclerosis By Skewing The Immune Response Toward An Antiinflammatory Profile, Esther Lutgens, Dirk Lievens, Linda Beckers, Erwin Wijnands, Oliver Soehnlein, Alma Zernecke, Tom Seijkens, David Engel, Jack Cleutjens, Anna M. Keller, Shalin H. Naike, Louis Boon, Hafid Ait Oufella, Ziad Mallat, Cory L. Ahonen, Randolph J. Noelle, Menno P. De Winther, Mat J. Daemen, Erik A. Biessen, Christian Weber
Dartmouth Scholarship
The CD40–CD40 ligand (CD40L) signaling axis plays an important role in immunological pathways. Consequently, this dyad is involved in chronic inflammatory diseases, including atherosclerosis. Inhibition of CD40L in apolipoprotein E (Apoe)–deficient ( Apoe - / - ) mice not only reduced atherosclerosis but also conferred a clinically favorable plaque phenotype that was low in inflammation and high in fibrosis. Blockade of CD40L may not be therapeutically feasible, as long-term inhibition will compromise systemic immune responses. Conceivably, more targeted intervention strategies in CD40 signaling will have less deleterious side effects. We report that deficiency in hematopoietic CD40 reduces atherosclerosis and induces …