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Genetics of HUS: the impact of MCP, CFH, and IF mutations on clinical presentation, response to treatment, and outcome.
The presentation, the response to therapy, and the outcome of the disease are influenced by the genotype, which will translate into improved management and therapy of patients and will provide the way to design tailored treatments.
Activation of human CD4+ cells with CD3 and CD46 induces a T-regulatory cell 1 phenotype
It is shown that co-engagement of CD3 and the complement regulator CD46 in the presence of IL-2 induces a Tr1-specific cytokine phenotype in human CD4+ T cells, suggesting that the complement system has a previously unappreciated role in T-cell-mediated immunity and tolerance.
Human T regulatory cells can use the perforin pathway to cause autologous target cell death.
It is demonstrated that activated human CD4(+)CD25(+) natural Treg cells express granzyme A but very little granzyme B, which suggests that the perforin/granzyme pathway is one of the mechanisms that T Reg cells can use to control immune responses.
Hereditary angioedema: the clinical syndrome and its management.
Hereditary angioedema is manifested by attacks of swelling of the extremities, face, trunk, airway, or abdominal viscera, occurring spontaneously or secondary to trauma. It is inherited as an
Adenovirus Type 11 Uses CD46 as a Cellular Receptor
It is demonstrated that adenovirus type 11 (Ad11; of species B) binds to Chinese hamster ovary cells transfected with CD46 (membrane cofactor protein)-cDNA at least 10 times more strongly than to CHO cells trans infected with cDNAs encoding CAR or CD55 (decay accelerating factor).
Membrane cofactor protein (MCP or CD46) is a cellular pilus receptor for pathogenic Neisseria
Data show that MCP is a human cell‐surface receptor for piliated pathogenic Neisseria, as proved by demonstrating that piliated, but not non‐piliated, gonococci bound to CHO cells transfected with human MCP‐cDNA.
Control of the complement system.
The complement system is designed to allow rapid, efficient, unimpeded activation on an appropriate foreign target while regulatory proteins intervene to prevent three undesirable consequences of complement activation: excessive activation on a single target, fluid phase activation, and activation on self.
Membrane cofactor protein (MCP or CD46): newest member of the regulators of complement activation gene cluster.
This protein is of interest to immunologists and clinicians because of its role in regulation of the complement pathways and, therefore, inflammation in immune complex-mediated syndromes; to reproductive immunologists on account of its expression on sperm and at the maternal-fetal interface; and to tumor immunologists because ofIts high expression on malignant cells.
Plasma complement components and activation fragments: associations with age-related macular degeneration genotypes and phenotypes.
Results implicate ongoing activation of the alternative complement pathway in AMD pathogenesis and increase levels of activation fragments Bb and C5a are independently associated with AMD.
Differential expression of granzymes A and B in human cytotoxic lymphocyte subsets and T regulatory cells.
Cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells use the perforin/granzyme pathway as a major mechanism to kill pathogen-containing cells and tumor cells.(1,2) Dysregulation of this