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Characterization of the baboon responses to Shiga-like toxin: descriptive study of a new primate model of toxic responses to Stx-1.
Mimicry and Antibody-Mediated Cell Signaling in Autoimmune Myocarditis1
- Ya Li, J. Heuser, L. Cunningham, S. Kosanke, M. Cunningham
- Biology, MedicineThe Journal of Immunology
- 1 December 2006
This work shows that autoantibodies to CM in anti-CM sera and mAbs derived from experimental autoimmune myocarditis targeted the heart cell surface and induced Ab-mediated cAMP-dependent protein kinase A activity.
The endothelial cell protein C receptor aids in host defense against Escherichia coli sepsis.
It is concluded that protein C/activated protein C binding to EPCR contributes to the negative regulation of the coagulopathic and inflammatory response to E coli and that E PCR provides an additional critical step in the host defense against E coli.
Pathogenic mechanisms in rheumatic carditis: focus on valvular endothelium.
- S. Roberts, S. Kosanke, Terrence Dunn S, D. Jankelow, C. M. Durán, M. Cunningham
- Biology, MedicineThe Journal of infectious diseases
- 1 February 2001
Evidence suggested that the pathogenesis of rheumatic heart disease involved the activation of surface valvular endothelium with the expression of VCAM-1 and the extravasation of CD4(+) and CD8(+) lymphocytes through the activated endothelia into the valve.
Delayed xenograft rejection of pig-to-baboon cardiac transplants after cobra venom factor therapy.
The findings indicate that the features of delayed xenograft rejection described in small animal models also occur in the pig-to-baboon model, and that rejection may occur in a complement-independent manner from the effects of antibody and/or host macrophages.
Cardiac myosin-Th17 responses promote heart failure in human myocarditis.
This translational study explains how an immune phenotype may be initiated by cardiac myosin TLR ligand stimulation of monocytes to generate Th17-promoting cytokines and development of pathogenic Th17 cells in human myocarditis and heart failure, and provides a rationale for targeting IL-17A as a therapeutic option.
Induction of Autoimmune Valvular Heart Disease by Recombinant Streptococcal M Protein
- A. Quinn, S. Kosanke, V. Fischetti, S. Factor, M. Cunningham
- Biology, MedicineInfection and Immunity
- 1 June 2001
The study demonstrates that the Lewis rat is a model of valvular heart disease and that streptococcal M protein can induce an autoimmune cell-mediated immune attack on the heart valve in an animal model, and supports the hypothesis that a bacterial antigen can break immune tolerance in vivo.
Group A streptococcal bacteremia: the role of tumor necrosis factor in shock and organ failure.
Anti-TNF- alpha monoclonal antibody treatment markedly improved mean arterial blood pressure, tissue perfusion, and survival, suggesting that TNF-alpha plays an important role in the induction of shock and organ failure in group A streptococcal bacteremia.
SPECIFIC INTRAVENOUS CARBOHYDRATE THERAPY A NEW CONCEPT IN INHIBITING ANTIBODY‐MEDIATED REJECTION—EXPERIENCE WITH ABO‐INCOMPATIBLE CARDIAC ALLOGRAFTING IN THE BABOON
“Accommodation” would appear to have developed in several baboons as graft function continued for periods of up to 39 days after discontinuation of carbohydrate therapy, which should allow organ allografting to be performed across the ABO blood group barrier in humans.
Lethal Staphylococcus aureus-induced shock in primates: prevention of death with anti-TNF antibody.
Treatment with MAb to TNF prevented multiple organ failure and achieved permanent (> 7 day) survival of all baboons.