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Prophylaxis And Therapy Of Inhalational Anthrax By A Novel Monoclonal Antibody To Protective Antigen That Mimics Vaccine-Induced Immunity, Laura Vitale, Diann Blanset, Israel Lowy, Thomas O'Neill, Joel Goldstein, Stephen F. Little, Gerard P. Andrews, Gary Dorough, Ronald K. Taylor, Tibor Keler
Prophylaxis And Therapy Of Inhalational Anthrax By A Novel Monoclonal Antibody To Protective Antigen That Mimics Vaccine-Induced Immunity, Laura Vitale, Diann Blanset, Israel Lowy, Thomas O'Neill, Joel Goldstein, Stephen F. Little, Gerard P. Andrews, Gary Dorough, Ronald K. Taylor, Tibor Keler
Dartmouth Scholarship
The neutralizing antibody response to the protective antigen (PA) component of anthrax toxin elicited by approved anthrax vaccines is an accepted correlate for vaccine-mediated protection against anthrax. We reasoned that a human anti-PA monoclonal antibody (MAb) selected on the basis of superior toxin neutralization activity might provide potent protection against anthrax. The fully human MAb (also referred to as MDX-1303 or Valortim) was chosen from a large panel of anti-PA human MAbs generated using transgenic mice immunized with recombinant PA solely on the basis of in vitro anthrax toxin neutralization. This MAb was effective in prophylactic and postsymptomatic treatment of …
The Role Of Cd4 T Cells In The Pathogenesis Of Murine Aids, Wen Li, William R. Green
The Role Of Cd4 T Cells In The Pathogenesis Of Murine Aids, Wen Li, William R. Green
Dartmouth Scholarship
LP-BM5, a retroviral isolate, induces a disease featuring retrovirus-induced immunodeficiency, designated murine AIDS (MAIDS). Many of the features of the LP-BM5-induced syndrome are shared with human immunodeficiency virus-induced disease. For example, CD4 T cells are critical to the development of MAIDS. In vivo depletion of CD4 T cells before LP-BM5 infection rendered genetically susceptible B6 mice MAIDS resistant. Similarly, MAIDS did not develop in B6.nude mice. However, if reconstituted with CD4 T cells, B6.nude mice develop full-blown MAIDS. Our laboratory has shown that the interaction of B and CD4 T cells that is central to MAIDS pathogenesis requires ligation of …