The association of anti-annexin1 antibodies with the occurrence of skin lesions in systemic lupus erythematosus

Meng, Zhen; Zr, Shi; Gz, Tan; Yin, Jun; Wu, Jingui; Xb, Mi; Wang, L

doi:10.1177/0961203313513820

Cited by 12 publications

(7 citation statements)

References 11 publications

(17 reference statements)

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“…Kretz et al [ 34 ] first described the association of anti-Annexin A1 antibodies with cutaneous lupus erythematosus in a large population of patients and, in particular, in those with discoid lesions. Serum anti-Annexin A1 IgG and IgM were subsequently studied in two small cohorts of Chinese patients with SLE (with and without skin lesions) by Meng et al [ 38 ] who, however, did not confirm the original finding and reported higher levels of both anti-Annexin A1 IgG and IgM in healthy controls than in SLE. The different ethnicity of the populations studied, and technical problems related to enzyme-linked immunosorbent assay (ELISA), limit the value of the studies above and do not allow a conclusion on any association of anti-Annexin A1 antibodies with cutaneous lupus.…”

Section: Anti-annexin A1 Antibodies: What Is Knownmentioning

confidence: 99%

Annexin A1 and Autoimmunity: From Basic Science to Clinical Applications

Bruschi

Petretto

Vaglio

et al. 2018

IJMS

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Annexin A1 is a protein with multifunctional roles in innate and adaptive immunity mainly devoted to the regulation of inflammatory cells and the resolution of inflammation. Most of the data regarding Annexin A1 roles in immunity derive from cell studies and from mice models lacking Annexin A1 for genetic manipulation (Annexin A1−/−); only a few studies sought to define how Annexin A1 is involved in human diseases. High levels of anti-Annexin A1 autoantibodies have been reported in systemic lupus erythematosus (SLE), suggesting this protein is implicated in auto-immunity. Here, we reviewed the evidence available for an association of anti-Annexin A1 autoantibodies and SLE manifestations, in particular in those cases complicated by lupus nephritis. New studies show that serum levels of Annexin A1 are increased in patients presenting renal complications of SLE, but this increment does not correlate with circulating anti-Annexin A1 autoantibodies. On the other hand, high circulating Annexin A1 levels cannot explain per se the development of autoantibodies since post-translational modifications are necessary to make a protein immunogenic. A hypothesis is presented here and discussed regarding the possibility that Annexin A1 undergoes post-translational modifications as a part of neutrophil extracellular traps (NETs) that are produced in response to viral, bacterial, and/or inflammatory triggers. In particular, focus is on the process of citrullination of Annexin A1, which takes place within NETs and that mimics, to some extent, other autoimmune conditions, such as rheumatoid arthritis, that are characterized by the presence of anti-citrullinated peptides in circulation. The description of pathologic pathways leading to modification of Annexin A1 as a trigger of autoimmunity is a cognitive evolution, but requires more experimental data before becoming a solid concept for explaining autoimmunity in human beings.

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Section: Anti-annexin A1 Antibodies: What Is Knownmentioning

confidence: 99%

Annexin A1 and Autoimmunity: From Basic Science to Clinical Applications

Bruschi

Petretto

Vaglio

et al. 2018

IJMS

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“…In the skin under normal conditions, the expression of AnxA1 is reduced [24], however, abnormal distribution and expression of the protein have been observed in inflammations and skin tumors [24–27] and mucosal injury [28–30]. The AnxA1 is strongly expressed in skin lesions in lupus [27], in differentiated squamous cell carcinoma [24] and melanoma [26].…”

Section: Introductionmentioning

confidence: 99%

“…The AnxA1 is strongly expressed in skin lesions in lupus [27], in differentiated squamous cell carcinoma [24] and melanoma [26]. In patients infected with Leishmania braziliensis , the expression of AnxA1 was stronger in macrophages CD163+ and lymphocytes CD4+ and CD8+ on infected skin compared to normal skin [31].…”

Section: Introductionmentioning

confidence: 99%

Heterogeneity of mast cells and expression of Annexin A1 protein in a second degree burn model with silver sulfadiazine treatment

et al. 2017

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Mast cells (MCs) participate in all stages of skin healing and one of their mediators is the Annexin A1 protein (AnxA1), linked to inflammation, proliferation, migration and apoptosis processes, but not studied in thermal burns yet. Therefore, our objectives were to evaluate the behavior of MCs and AnxA1 in a second degree burn model, treated or not with silver sulfadiazine 1% (SDP 1%) and associated to macrophages quantification and cytokines dosages. MCs counts showed few cells in the early stages of repair but increased MCs in the final phases in the untreated group. The normal skin presented numerous tryptase-positive MCs that were reduced after burning in all analyzed periods. Differently, few chymase-positive MCs were observed in the early stages of healing, however, increased chymase-positive MCs were found at the final phase in the untreated group. MCs also showed high immunoreactivity for AnxA1 on day 3 in both groups. In the tissue there was a strong protein expression in the early stages of healing, but in the final phases only in the SDP treated animals. TNF-α, IL-1β, IL-6, IL-10 and MCP-1 levels and macrophages quantification were increased in inflammation and reepithelialization phases. Reduced IL-1β, IL-6 and IL-10 levels and numerous macrophages occurred in the treated animals during tissue repair. Our results indicate modulation in the profile of MCs and AnxA1expression during healing by the treatment with SDP 1%, pointing them as targets for therapeutic interventions on skin burns.

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“…Details of the specific antibodies and recombinant proteins that were used in the study are available from the author upon request. Immunoblot assays with human foreskin tissue lysate, recombinant proteins, and purified proteins as antigens were performed as previously described (). For protein identification, human foreskin lysate was run on 2‐dimensional electrophoresis gels, as previously described (), stained with Coomassie blue, or transferred onto PVDF membranes (Millipore) to blot with patient serum.…”

Section: Methodsmentioning

confidence: 99%

Association of Anti–Acidic Ribosomal Protein P0 and Anti–Galectin 3 Antibodies With the Development of Skin Lesions in Systemic Lupus Erythematosus

Shi

Tan

Meng

et al. 2014

Arthritis & Rheumatology

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Objective. The specific autoantibodies and antigens that mediate systemic lupus erythematosus (SLE)-related organ injuries remain largely unknown. This study was undertaken to investigate the antibodymediated immune response that leads to SLE skin lesions.Methods. The study included 85 SLE patients with lupus-specific skin lesions and 31 without skin lesions. The reactivity of serum antibody with skin antigens was determined by immunoblotting using human foreskin as the substrate. Skin antigens were identified using mass spectrometry. Serum antibody was isolated by affinity purification and was injected intracutaneously into mouse skin to determine pathogenicity. Serum antibody levels were monitored by enzyme-linked immunosorbent assay.Results. We determined that 78% of the patients with skin lesions had serum antibodies reactive with 35-kd and/or 25-kd skin antigens, which was significantly higher than the percentage of patients without skin lesions (P < 0.0001), suggesting a correlation between immune response and skin lesions. Acidic ribosomal protein P0 (RPLP0) and galectin 3 were 2 target antigens identified from 35-kd and 25-kd proteins, respectively. Purified serum anti-RPLP0 and anti-galectin 3 antibodies induced lupus-like histologic changes after intracutaneous injection. Anti-RPLP0 and anti-galectin 3 antibody levels were significantly higher in SLE patients than in healthy controls and decreased with skin recovery. Anti-galectin 3 antibody levels were not significantly higher in SLE patients than in patients with dermatomyositis or scleroderma, but strongly related to lupus cutaneous vasculitis. Additionally, levels of the 2 antibodies were positively correlated with leukopenia and C3 deficiency, and the anti-RPLP0 antibody level was also positively correlated with arthritis and SLE disease activity. Conclusion. Our findings indicate that the immune response mediated by serum anti-RPLP0 and anti-galectin 3 antibodies plays a key role in the pathogenesis of SLE skin lesions. These findings provide new insights into the mechanism of SLE-related organ disorders.Systemic lupus erythematosus (SLE) is a unique autoimmune disease characterized by extremely heterogeneous clinical manifestations and the most complex autoantibody profile (1-5). Autoantibodies not only serve as a marker of disease diagnosis, activity, and severity (6,7), but they also play a primary and pivotal role in the initiation and exacerbation of SLE disease (8,9). A cluster of anti-nuclear debris antibodies, including anti-double-stranded DNA (anti-dsDNA), anti-

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The association of anti-annexin1 antibodies with the occurrence of skin lesions in systemic lupus erythematosus

Cited by 12 publications

References 11 publications

Annexin A1 and Autoimmunity: From Basic Science to Clinical Applications

Annexin A1 and Autoimmunity: From Basic Science to Clinical Applications

Heterogeneity of mast cells and expression of Annexin A1 protein in a second degree burn model with silver sulfadiazine treatment

Association of Anti–Acidic Ribosomal Protein P0 and Anti–Galectin 3 Antibodies With the Development of Skin Lesions in Systemic Lupus Erythematosus

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