Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Complement and : Early Complement-Dependent Events Are Important for DC Migration and Protection During Mouse Lung Infection.
Front Immunol
June 2021
Medical School Hannover, Institute of Medical Microbiology and Hospital Epidemiology, Hannover, Germany.
The zoonotic intracellular bacterium causes life-threatening pneumonia in humans. During mouse lung infection, complement factor C3 and the anaphylatoxin C3a augment protection against by a so far unknown mechanism. To clarify how complement contributes to the early, innate and the late, specific immune response and resulting protection, this study addresses the amount of C3, the timing when its presence is required as well as the anaphylatoxin receptor(s) mediating its effects and the complement-dependent migration of dendritic cells.
View Article and Find Full Text PDFAbsence of a neutralizing antibody response to humanized cobra venom factor in mice.
Mol Immunol
May 2018
INSERM, UMRS 1138, Centre de Recherche des Cordeliers, Paris, 75006 France.
Cobra venom factor (CVF) is the complement-activating protein in cobra venom. Humanized CVF (hCVF) is a human C3 derivative where the C-terminal 168 amino acid residues were replaced with the homologous sequence from CVF. hCVF has been shown in multiple models of disease with complement pathology to be a promising therapeutic agent, with no observed adverse effects.
View Article and Find Full Text PDFHumanized cobra venom factor decreases myocardial ischemia-reperfusion injury.
Mol Immunol
December 2009
Center for Experimental Therapeutics and Reperfusion Injury, Brigham and Women's Hospital, Harvard School of Medicine, 75 Francis Street, Boston, MA 02115, USA.
Cobra venom factor (CVF) is a complement activating protein in cobra venom, which functionally resembles C3b, and has been used for decades for decomplementation of serum to investigate the role of complement in many model systems of disease. The use of CVF for clinical practice is considered impractical because of immunogenicity issues. Humanization of CVF was recently demonstrated to yield a potent CVF-like molecule.
View Article and Find Full Text PDFTransient decomplementation of mice delays onset of experimental autoimmune encephalomyelitis and impairs MOG-specific T cell response and autoantibody production.
Mol Immunol
November 2009
Department of Immunology, Eötvös Loránd University, H-1117 Budapest, Hungary.
Multiple sclerosis (MS) is the most common inflammatory and demyelinating disease of the central nervous system. In both MS and its animal model experimental autoimmune encephalomyelitis (EAE), it is thought that infiltrating CD4(+) T cells initiate an inflammatory process and collect other immune effectors to mediate tissue damage. The pathophysiology of the disease however remains unclear.
View Article and Find Full Text PDFEarly cytokine profiles in the joint define pathogen clearance and severity of arthritis in Chlamydia-induced arthritis in rats.
Arthritis Rheum
February 2006
Toronto Western Research Institute, University of Toronto, Toronto, Ontario, Canada.
Objective: Although Chlamydia trachomatis-induced arthritis is among the most common rheumatic diseases having an identified infectious trigger, the pathogenesis of this arthritis is not well defined. We sought to investigate the host-microbe interactions that contribute to the severity of arthritis initiated by chlamydial infection.
Methods: We established an experimental rat model of C.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!