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2014 ; 176
(3
): 341-50
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Endogenous interleukin (IL)-17A promotes pristane-induced systemic autoimmunity
and lupus nephritis induced by pristane
#MMPMID24528105
Summers SA
; Odobasic D
; Khouri MB
; Steinmetz OM
; Yang Y
; Holdsworth SR
; Kitching AR
Clin Exp Immunol
2014[Jun]; 176
(3
): 341-50
PMID24528105
show ga
Interleukin (IL)-17A is increased both in serum and in kidney biopsies from
patients with lupus nephritis, but direct evidence of pathogenicity is less well
established. Administration of pristane to genetically intact mice results in the
production of autoantibodies and proliferative glomerulonephritis, resembling
human lupus nephritis. These studies sought to define the role of IL-17A in
experimental lupus induced by pristane administration. Pristane was administered
to wild-type (WT) and IL-17A(-/-) mice. Local and systemic immune responses were
assessed after 6?days and 8?weeks, and autoimmunity, glomerular inflammation and
renal injury were measured at 7?months. IL-17A production increased significantly
6?days after pristane injection, with innate immune cells, neutrophils (Ly6G(+))
and macrophages (F4/80(+)) being the predominant source of IL-17A. After 8?weeks,
while systemic IL-17A was still readily detected in WT mice, the levels of
proinflammatory cytokines, interferon (IFN)-? and tumour necrosis factor (TNF)
were diminished in the absence of endogenous IL-17A. Seven months after pristane
treatment humoral autoimmunity was diminished in the absence of IL-17A, with
decreased levels of immunoglobulin (Ig)G and anti-dsDNA antibodies. Renal
inflammation and injury was less in the absence of IL-17A. Compared to WT mice,
glomerular IgG, complement deposition, glomerular CD4(+) T cells and intrarenal
expression of T helper type 1 (Th1)-associated proinflammatory mediators were
decreased in IL-17A(-/-) mice. WT mice developed progressive proteinuria, but
functional and histological renal injury was attenuated in the absence of IL-17A.
Therefore, IL-17A is required for the full development of autoimmunity and lupus
nephritis in experimental SLE, and early in the development of autoimmunity,
innate immune cells produce IL-17A.
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