Molecular mimicry in systemic lupus erythematosus

Agmon‐Levin, Nancy; Blank, Miri; Paz, Ziv; Shoenfeld, Yehuda

doi:10.1177/0961203309346653

Cited by 44 publications

(27 citation statements)

References 54 publications

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“…Systemic lupus erythematosus (SLE) is an autoimmune disorder that occurs in multiple organs characterized with autoantibody production [1][2][3]. In typical SLE, the immune system is aberrantly activated to attack tissue from self as autoantigens, resulting in production of autoantibody and generation of a vicious cycle of chronic inflammation and tissue damage [1][2][3].…”

Section: Introductionmentioning

confidence: 99%

“…In typical SLE, the immune system is aberrantly activated to attack tissue from self as autoantigens, resulting in production of autoantibody and generation of a vicious cycle of chronic inflammation and tissue damage [1][2][3]. Although it is traditionally believed that lymphocyte abnormalities are the major pathological bases for SLE [1][2][3], recent studies have shown the evidence of the involvement of monocytes/macrophages in the pathogenesis of the disease [4][5][6].…”

Section: Introductionmentioning

confidence: 99%

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TIPE2 Alleviates Systemic Lupus Erythematosus Through Regulating Macrophage Polarization

Xian

Yang

et al. 2016

Cell Physiol Biochem

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Background/Aims: We have recently shown that macrophage polarization may alter the pathogenesis and severity of systemic lupus erythematosus (SLE). However, a practical approach to modulate macrophage polarization in vivo is so far not available. In the current study, we aimed to use tumor necrosis factor (TNF)-alpha-induced protein 8-like 2 (TIPE2) to regulate macrophage polarization in vitro and in vivo, and to study the effects on experimental SLE. Methods: We prepared adeno-associated virus carrying TIPE2 (AAV-TIPE2). We induced experimental SLE in mice with an activated lymphocyte-derived DNA (ALD-DNA) method. We examined the effects of TIPE2 overexpression on macrophage polarization in vitro, and in vivo in the SLE model. We also examined the effects of TIPE2 overexpression on the severity of SLE, by serum anti-dsDNA autoantibody, renal pathological changes, and urine protein levels. Results: ALD-DNA induced SLE-like features in mice, manifested by induction of serum anti-dsDNA autoantibody, renal pathological changes, and increases in urine protein levels. TIPE2 overexpression by AAV-TIPE2 induced macrophage polarization to a M2 phenotype, in vitro and in vivo in the SLE mouse model. TIPE2 overexpression significantly decreased SLE severity. Conclusion: TIPE2 alleviates experimental SLE through induction of macrophage polarization to a M2 phenotype, which may be used as a promising therapeutic strategy for treating SLE.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

TIPE2 Alleviates Systemic Lupus Erythematosus Through Regulating Macrophage Polarization

Xian

Yang

et al. 2016

Cell Physiol Biochem

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“…A hypothesis might be that these antibodies are secreted against pathogen cell surface GalNaccontaining glycoconiugates cross-reacting with GdIgA1, realizing a molecular mimicry [68] . A prevalence of IgA1 autoantibody response [61] anti GdIgA1 may justify the fact that some patients have only IgA1 antibody in the glomeruli [69] .…”

Section: Salvadori M Et Al Pathophysiology Of Nephropathymentioning

confidence: 99%

Update on immunoglobulin A nephropathy, Part I: Pathophysiology

Salvadori

Rosso

2015

WJN

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Immunoglobulin A (IgA) nephropathy is one of the most common glomerulonephritis and its frequency is probably underestimated because in most patients the disease has an indolent course and the kidney biopsy is essential for the diagnosis. In the last years its pathogenesis has been better identified even if still now several questions remain to be answered. The genetic wide association studies have allowed to identifying the relevance of genetics and several putative genes have been identified. The genetics has also allowed explaining why some ancestral groups are affected with higher frequency. To date is clear that IgA nephropathy is related to auto antibodies against immunoglobulin A1 (IgA1) with poor O-glycosylation. The role of mucosal infections is confirmed, but which are the pathogens involved and which is the role of Toll-like receptor polymorphism is less clear. Similarly to date whether the disease is due to the circulating immunocomplexes deposition on the mesangium or whether the antigen is already present on the mesangial cell as a "lanthanic" deposition remains to be clarified. Finally also the link between the mesangial and the podocyte injury and the tubulointerstitial scarring, as well as the mechanisms involved need to be better clarified.

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“…Numerous infectious agents have been related to autoimmunity and production of autoantibodies [20][21][22] as well as with evident diseases such as SLE and APS [23][24][25][26][27]. Additional factors such as hormones [28,29], vitamins such as vitamin D [30][31][32], sun exposure, etc.…”

mentioning

confidence: 99%