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IgE in the Pathogenesis of SLE: From Pathogenic Role to Therapeutic Target.

ABSTRACT: Systemic lupus erythematosus (SLE) is a multifactorial chronic autoimmune disease, marked by the presence of autoantibodies to nuclear antigens belonging to different isotype classes. For several years, IgE antibodies have been incriminated in the development of allergic diseases and parasitic infections and different anti-IgE therapies have been developed to encounter the pathogenic role of IgE in these pathologies. Recently, multiple studies showed the presence of elevated total IgE levels and demonstrated a pathogenic role of autoreactive IgE in SLE. This review aims to summarize the findings incriminating IgE and autoreactive IgE in the pathophysiology of SLE, to describe their functional outcomes on their targeted cells as well as to discuss different IgE-related therapeutic modalities that emerged and that may be beneficial for SLE patient care.

SUBMITTER: Lamri Y

PROVIDER: S-EPMC7768355 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature

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IgE in the Pathogenesis of SLE: From Pathogenic Role to Therapeutic Target.

Lamri Yasmine Y Charles Nicolas N

Antibodies (Basel, Switzerland) 20201208 4

Systemic lupus erythematosus (SLE) is a multifactorial chronic autoimmune disease, marked by the presence of autoantibodies to nuclear antigens belonging to different isotype classes. For several years, IgE antibodies have been incriminated in the development of allergic diseases and parasitic infections and different anti-IgE therapies have been developed to encounter the pathogenic role of IgE in these pathologies. Recently, multiple studies showed the presence of elevated total IgE levels and ...[more]

PMID: 33302566

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Project description:The present study aimed to reveal the metabolic alterations of the extracellular matrix (ECM) in uterosacral ligament (USL) with pelvic organ prolapse (POP) and to explore the role of transforming growth factor??1 (TGF??1) in pathogenesis of POP. For this purpse, 60 participants who underwent hysterectomy for benign indications were enrolled, 30 of which had symptomatic POP (grade II, III or IV) and composed the POP group, and the other 30 had asymptomatic POP (grade I or less) and served as the controls. Collagen fibers, elastin,matrix metalloproteinase (MMP)?2/9, tissue inhibitor of matrix metalloproteinases (TIMP)?2 and TGF??1 were examined by Masson's trichrome staining, immunohistochemistry and RT-qPCR using USL biopsies. In vitro, human USL fibroblasts (hUSLFs) were primary cultured, pre-treated with recombinant TGF??1 (0, 5, or 10 ng/ml) and then subjected to cyclic mechanical stretching (CMS; 0 or 5,333 µ? strain). Changes in the expression levels of collagen type I/III, elastin, TIMP?2, MMP?2/9 and Smad were detected. Our results revealed that at the tissue level, the expression of collagen fibers, elastin, TIMP?2 and TGF??1 was significantly reduced in the POP group, while the activities of MMP?2/9 were significantly upregulated, compared with the control group. Statistical analysis indicated that the mRNA expression of TGF??1 inversely correlated with the severity of POP partially. Our in vitro experimental data demonstrated that a CMS of 5333 µ? strain promoted the degradation of ECM proteins, inhibited the synthesis of TIMP?2, and upregulated the proteolytic activities of MMP?2/9. Pre-treatment with TGF??1 attenuated the loss of ECM by stimulating the synthesis of TIMP?2 and inhibiting the activities of MMP?2/9 through the TGF??1/Smad3 signaling pathway. On the whole, our data indicate that the reduced anabolism and increased catabolism of ECM proteins in USL are the pathological characteristics of POP. TGF??1 not only has a specific value in predicting the severity of POP, but should also be considered as a novel therapeutic target for POP.

Dataset Information

IgE in the Pathogenesis of SLE: From Pathogenic Role to Therapeutic Target.

Publications

IgE in the Pathogenesis of SLE: From Pathogenic Role to Therapeutic Target.

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