Effects of adjuvants for human use in systemic lupus erythematosus (SLE)-prone (New Zealand black/New Zealand white) F1 mice

Favoino, Elvira; Favia, E. I.; Digiglio, Liboria; Racanelli, Vito; Shoenfeld, Yehuda; Perosa, Federico

doi:10.1111/cei.12208

Cited by 14 publications

(4 citation statements)

References 56 publications

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“…This datum is consistent with both evidence from clinical case reports [30,103,[105][106][107][108][109][110] and data from murine models where different adjuvants, such as Alum and MF59 [111][112][113][114][115] were characterised by several mechanisms of action.…”

Section: Accepted Manuscriptsupporting

confidence: 88%

On vaccine's adjuvants and autoimmunity: Current evidence and future perspectives

Pellegrino

Clementi

Radice

2015

Autoimmunity Reviews

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Section: Accepted Manuscriptsupporting

confidence: 88%

On vaccine's adjuvants and autoimmunity: Current evidence and future perspectives

Pellegrino

Clementi

Radice

2015

Autoimmunity Reviews

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“…Furthermore, a similar spectrum of autoantibodies has been reported following exposure to squalene, however less efficiently than with pristane. 82,83 Finally, SLE can be induced by diverse adjuvants including various vaccines as well as silicone implantation. Therefore, there is a need to be mindful of such associations in order to recognize those individuals at high risk who might undergo preventive measures.…”

Section: Asia Syndrome and Slementioning

confidence: 99%

Autoimmune/inflammatory syndrome induced by adjuvants (Shoenfeld’s syndrome) – An update

Watad

Quaresma

Brown

et al. 2017

Lupus

Self Cite

124

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Autoimmune/inflammatory syndrome induced by adjuvants (ASIA) has been widely described in many studies conducted thus far. The syndrome incorporates five immune-mediated conditions, all associated with previous exposure to various agents such as vaccines, silicone implants and several others. The emergence of ASIA syndrome is associated with individual genetic predisposition, for instance those carrying HLA-DRB1*01 or HLA-DRB4 and results from exposure to external or endogenous factors triggering autoimmunity. Such factors have been demonstrated as able to induce autoimmunity in both animal models and humans via a variety of proposed mechanisms. In recent years, physicians have become more aware of the existence of ASIA syndrome and the relationship between adjuvants exposure and autoimmunity and more cases are being reported. Accordingly, we have created a registry that includes at present more than 300 ASIA syndrome cases that have been reported by different physicians worldwide, describing various autoimmune conditions induced by diverse adjuvants. In this review, we have summarized the updated literature on ASIA syndrome and the knowledge accumulated since 2013 in order to elucidate the association between the exposure to various adjuvant agents and its possible clinical manifestations. Furthermore, we especially referred to the relationship between ASIA syndrome and systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS).

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“…Other oil adjuvants such as (Incomplete Freund's adjuvant, IFA) and squalene (MF59) have been shown to induce lupus-related autoantibodies in non-autoimmune mice [ 11 ]. Recently, IFA have been shown to accelerate the onset and progression of proteinuria in BWF1 mice [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Pristane-Accelerated Autoimmune Disease in (SWR X NZB) F1 Mice Leads to Prominent Tubulointerstitial Inflammation and Human Lupus Nephritis-Like Fibrosis

et al. 2016

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Mouse models lupus nephritis (LN) have provided important insights into disease pathogenesis, although none have been able to recapitulate all features of the human disease. Using comprehensive longitudinal analyses, we characterized a novel accelerated mouse model of lupus using pristane treatment in SNF1 (SWR X NZB F1) lupus prone mice (pristane-SNF1 mice). Pristane treatment in SNF1 mice accelerated the onset and progression of proteinuria, autoantibody production, immune complex deposition and development of renal lesions. At week 14, the pristane-SNF1 model recapitulated kidney disease parameters and molecular signatures seen in spontaneous disease in 36 week-old SNF1 mice and in a traditional IFNα-accelerated NZB X NZW F1 (BWF1) model. Blood transcriptome analysis revealed interferon, plasma cell, neutrophil, T-cell and protein synthesis signatures in the pristane-SNF1 model, all known to be present in the human disease. The pristane-SNF1 model appears to be particularly useful for preclinical research, robustly exhibiting many characteristics reminiscent of human disease. These include i) a stronger upregulation of the cytosolic nucleic acid sensing pathway, which is thought to be key component of the pathogenesis of the human disease, and ii) more prominent kidney interstitial inflammation and fibrosis, which have been both associated with poor prognosis in human LN. To our knowledge, this is the only accelerated model of LN that exhibits a robust tubulointerstitial inflammatory and fibrosis response. Taken together our data show that the pristane-SNF1 model is a novel accelerated model of LN with key features similar to human disease.

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Effects of adjuvants for human use in systemic lupus erythematosus (SLE)-prone (New Zealand black/New Zealand white) F1 mice

Cited by 14 publications

References 56 publications

On vaccine's adjuvants and autoimmunity: Current evidence and future perspectives

On vaccine's adjuvants and autoimmunity: Current evidence and future perspectives

Autoimmune/inflammatory syndrome induced by adjuvants (Shoenfeld’s syndrome) – An update

Pristane-Accelerated Autoimmune Disease in (SWR X NZB) F1 Mice Leads to Prominent Tubulointerstitial Inflammation and Human Lupus Nephritis-Like Fibrosis

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