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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Contrib+Nephrol
2011 ; 169
(ä): 211-220
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Experimental models of vasculitis and glomerulonephritis induced by
antineutrophil cytoplasmic autoantibodies
#MMPMID21252521
Jennette JC
; Xiao H
; Falk R
; Gasim AMH
Contrib Nephrol
2011[]; 169
(ä): 211-220
PMID21252521
show ga
Antineutrophil cytoplasmic autoantibodies (ANCA) are closely associated with
systemic small vessel vasculitis characterized by segmental vessel wall
necrotizing inflammation and a paucity of immunoglobulin deposition. Clinically,
in vitro and experimental animal model observations indicate a direct pathogenic
role for ANCA. This review focuses on the results of experiments utilizing a
mouse model of ANCA disease induced by transfer of mouse anti-MPO IgG or anti-MPO
lymphocytes into recipient mice, which causes small vessel vasculitis and
glomerulonephritis that closely mimics human disease. Evidence for the following
conclusion about this model, and by implication about human ANCA disease, will be
summarized as follows: (1) anti-MPO IgG is sufficient even in the absence of
functional T cells to cause disease and anti-MPO T lymphocytes are not sufficient
to cause acute injury; (2) neutrophils are required; (3) ANCA antigens in bone
marrow-derived cells are sufficient targets; (4) increased circulating
pro-inflammatory cytokines and microbial products exacerbate disease, and
concurrent viral infection exacerbates and modulates the phenotype of disease;
(5) Fc? receptor engagement is required for disease induction, and Fc? receptor
repertoire modulates the phenotype of disease, especially pulmonary disease; (6)
activation of the alternative pathway of complement is required, complement is
activated by factors released by neutrophils stimulated by ANCA IgG and
engagement of C5a receptors is a primary event in complement-mediated
amplification; and (7) genetic background has a marked influence on the severity
and outcome of disease, and modified gene expression in bone marrow-derived cells
is the primary basis for genetically determined differences in disease
susceptibility. Investigations using this animal model of ANCA disease have
provided important insights into the cellular, molecular and genetic factors
involved in the pathogenesis of ANCA disease which are likely to lead to the
identification of improved markers of disease activity and response to therapy,
as well as more effective and less toxic therapies.
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