Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that mostly affects women. Patients with SLE typically exhibit a broad defect in immune tolerance, most conspicuously demonstrated by the presence of antibodies against intranuclear and intercellular molecules, particularly nucleic acid-protein complexes. Loss of tolerance allows the development of a chronic autoimmune response that produces autoantibodies and activated self-reactive T cells that cause inflammation in susceptible vascular beds and target organs. Autoantibodies appear and gradually accrue until target organ inflammation signals the clinical onset of a heterogeneous disease that usually has a relapsing and remitting course.
In SLE, there is a limited connection between the titers and repertoire of autoantibodies and the clinical expression of the disease. In fact, autoantibodies are commonly present in patients that lack any evidence of disease activity. This implies that, although tolerance loss is probably a sine qua non event for the development of disease, other factors determine the organs and tissues that will be involved, as well as the timing and severity of local inflammation.
At present we lack biomarkers to be able to predict which organs will be involved, when organ inflammation will occur, and how severe it will be. Therefore, there is an urgent need to gain a deeper understanding of disease pathogenesis and simultaneously identify cellular and molecular biomarkers that reflect systemic and local disease activity.
Background
Biomarkers can be useful tools in most diseases, but are urgently needed in SLE. From a clinical point of view, SLE is a very complex disease. Each clinical manifestation has its own pathogenesis, clinical course and prognosis. For example, tubule-interstitial inflammation is usually chronic in patients with lupus nephritis even when the disease is adequately controlled in other organs. Kidney biopsy remains the gold standard for evaluating renal inflammation in lupus. Therefore, a biomarker able to predict inflammation and remaining renal function remains a pressing need. On the other hand, disease heterogeneity, in terms of organ involvement and response to available therapies are usually dealt with in an empirical manner and biomarkers able to guide therapeutic choices and offer prognostic data would significantly improve clinical practice.
Goal
The aim of this Research Topic is to bring together work that explores possible biomarkers able to divide patients into disease subsets, predict systemic and/or organ-specific disease activity, and response of patients to established or novel therapies. Because we understand that the predictive capacity of biomarkers is intimately linked to disease processes, we would like to also welcome work that highlights molecules or genes whose function or expression could eventually indicate disease status. It is also important that we have data from human studies which utilize well characterized, preferably untreated patients and healthy and disease controls matched for age, gender, ethnicity etc.
This issue aims to investigate specific biomarkers that can be used in early determination of SLE or those at risk of disease, as well as data related to disease activity. We also welcome studies that explore biomarkers that can be utilized in the targeting of therapeutics. In this Research Topic, we welcome articles focusing on, but not limited to:
• Accumulation of specific cell types in SLE patients
• SLE specific antibodies in diagnostic or treatment
• Genes upregulated or downregulated in SLE
• Clinical disease markers used in predicting SLE outcomes
• Hormone profiles
• Multi-omics
• targeted and combined analysis of metabolites
• proteomics
• gene expression
• high resolution flow cytometry
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that mostly affects women. Patients with SLE typically exhibit a broad defect in immune tolerance, most conspicuously demonstrated by the presence of antibodies against intranuclear and intercellular molecules, particularly nucleic acid-protein complexes. Loss of tolerance allows the development of a chronic autoimmune response that produces autoantibodies and activated self-reactive T cells that cause inflammation in susceptible vascular beds and target organs. Autoantibodies appear and gradually accrue until target organ inflammation signals the clinical onset of a heterogeneous disease that usually has a relapsing and remitting course.
In SLE, there is a limited connection between the titers and repertoire of autoantibodies and the clinical expression of the disease. In fact, autoantibodies are commonly present in patients that lack any evidence of disease activity. This implies that, although tolerance loss is probably a sine qua non event for the development of disease, other factors determine the organs and tissues that will be involved, as well as the timing and severity of local inflammation.
At present we lack biomarkers to be able to predict which organs will be involved, when organ inflammation will occur, and how severe it will be. Therefore, there is an urgent need to gain a deeper understanding of disease pathogenesis and simultaneously identify cellular and molecular biomarkers that reflect systemic and local disease activity.
Background
Biomarkers can be useful tools in most diseases, but are urgently needed in SLE. From a clinical point of view, SLE is a very complex disease. Each clinical manifestation has its own pathogenesis, clinical course and prognosis. For example, tubule-interstitial inflammation is usually chronic in patients with lupus nephritis even when the disease is adequately controlled in other organs. Kidney biopsy remains the gold standard for evaluating renal inflammation in lupus. Therefore, a biomarker able to predict inflammation and remaining renal function remains a pressing need. On the other hand, disease heterogeneity, in terms of organ involvement and response to available therapies are usually dealt with in an empirical manner and biomarkers able to guide therapeutic choices and offer prognostic data would significantly improve clinical practice.
Goal
The aim of this Research Topic is to bring together work that explores possible biomarkers able to divide patients into disease subsets, predict systemic and/or organ-specific disease activity, and response of patients to established or novel therapies. Because we understand that the predictive capacity of biomarkers is intimately linked to disease processes, we would like to also welcome work that highlights molecules or genes whose function or expression could eventually indicate disease status. It is also important that we have data from human studies which utilize well characterized, preferably untreated patients and healthy and disease controls matched for age, gender, ethnicity etc.
This issue aims to investigate specific biomarkers that can be used in early determination of SLE or those at risk of disease, as well as data related to disease activity. We also welcome studies that explore biomarkers that can be utilized in the targeting of therapeutics. In this Research Topic, we welcome articles focusing on, but not limited to:
• Accumulation of specific cell types in SLE patients
• SLE specific antibodies in diagnostic or treatment
• Genes upregulated or downregulated in SLE
• Clinical disease markers used in predicting SLE outcomes
• Hormone profiles
• Multi-omics
• targeted and combined analysis of metabolites
• proteomics
• gene expression
• high resolution flow cytometry
