Ro60 and La ribonucleoproteins become self-aggregated by cell stress

Sánchez-Rodríguez, Sergio Hugo; Herrera-van-Oostdam, D.; Avalos‐Díaz, Esperanza; Herrera‐Esparza, Rafael

doi:10.4081/reumatismo.2007.292

Cited by 3 publications

(3 citation statements)

References 34 publications

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“…It has been found that UV-B-irradiated keratinocytes express nuclear and cytoplasmic antigens (SSA/Ro, RNP, and Sm) in the surface of the cell membrane [ 44 – 48 ]; this externalization might play a role in the exacerbation of skin symptoms. Cell redistribution of Ro60 and La caused by heat or UV radiation, and its interaction with cytoskeleton, is associated to HSP70 suggesting a connection to cellular stress [ 49 ].…”

Section: Uv Radiation and Slementioning

confidence: 99%

DNA Damage and Deficiencies in the Mechanisms of Its Repair: Implications in the Pathogenesis of Systemic Lupus Erythematosus

Mireles-Canales

González-Chávez

Quiñonez-Flores

et al. 2018

Journal of Immunology Research

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Systemic lupus erythematosus (SLE) is a perplexing and potentially severe disease, the pathogenesis of which is yet to be understood. SLE is considered to be a multifactorial disease, in which genetic factors, immune dysregulation, and environmental factors, such as ultraviolet radiation, are involved. Recently, the description of novel genes conferring susceptibility to develop SLE even in their own (monogenic lupus) has raised the interest in DNA dynamics since many of these genes are linked to DNA repair. Damage to DNA induces an inflammatory response and eventually triggers an immune response, including those targeting self-antigens. We review the evidence that indicates that patients with SLE present higher levels of DNA damage than normal subjects do and that several proteins involved in the preservation of the genomic stability show polymorphisms, some of which increase the risk for SLE development. Also, the experience from animal models reinforces the connection between DNA damage and defective repair in the development of SLE-like disease including characteristic features such as anti-DNA antibodies and nephritis. Defining the role of DNA damage response in SLE pathogenesis might be strategic in the quest for novel therapies.

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Section: Uv Radiation and Slementioning

confidence: 99%

DNA Damage and Deficiencies in the Mechanisms of Its Repair: Implications in the Pathogenesis of Systemic Lupus Erythematosus

Mireles-Canales

González-Chávez

Quiñonez-Flores

et al. 2018

Journal of Immunology Research

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“…This clinical manifestation may also attribute toward the specific downregulation of HSP27 in anti-ENA + patients. Recently, some studies have documented the association of HSP70 with ribonucleoprotein autoantigens (Ro/La) in SLE patients and have been shown to participate in the shuttling of these autoantigens to the dermo-epidermal junction on the cell surface [45,46] thus exposing the autoantigens. This in turn could evoke the immune response by generating autoantibodies against autoantigens [47].…”

Section: Discussionmentioning

confidence: 99%

Heat shock protein 27 and its regulatory molecules express differentially in SLE patients with distinct autoantibody profiles

et al. 2015

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“…A pro‐inflammatory role of HSP70 has been suggested for a number of human diseases including psoriasis (25,26) and lupus erythematosus (LE) (27–32). However, the role of HSP70 in the pathogenesis of inflammatory diseases remains ill defined and depends on the tissue microenvironment and the location of the chaperone (33).…”

Section: Introductionmentioning

confidence: 99%

Human keratinocytes release high levels of inducible heat shock protein 70 that enhances peptide uptake

Wang

Zeitvogel

Dressel

et al. 2011

Experimental Dermatology

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Ro60 and La ribonucleoproteins become self-aggregated by cell stress

Cited by 3 publications

References 34 publications

DNA Damage and Deficiencies in the Mechanisms of Its Repair: Implications in the Pathogenesis of Systemic Lupus Erythematosus

DNA Damage and Deficiencies in the Mechanisms of Its Repair: Implications in the Pathogenesis of Systemic Lupus Erythematosus

Heat shock protein 27 and its regulatory molecules express differentially in SLE patients with distinct autoantibody profiles

Human keratinocytes release high levels of inducible heat shock protein 70 that enhances peptide uptake

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