Pathogenesis of proliferative lupus nephritis from a historical and personal perspective

Fu, Shu Man; Wang, Hongyang; Dai, Chao; Sung, Sun‐Sang J.; Gaskin, Felicia

doi:10.1016/j.clim.2016.07.024

Cited by 10 publications

(5 citation statements)

References 29 publications

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“…Systemic lupus erythematosus (SLE) is an autoimmune disease initiated by Ab against a wide variety of self-antigens (Reviewed in (1–3)). The etiology of SLE is composed of both genetic and environmental components.…”

Section: Introductionmentioning

confidence: 99%

“…The etiology of SLE is composed of both genetic and environmental components. Two mouse strains utilizing the autoimmune (NZB × NZW)F1-derived sublines NZM2328 (NZM) and NZM2410 have been most useful in identifying lupus-associated genes in SLE (1, 4). The roles of many susceptibility genes in SLE-related immune response pathways have been studied (2, 4–6) while novel roles for other genes continue to be discovered (7).…”

Section: Introductionmentioning

confidence: 99%

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Dependence of Glomerulonephritis Induction on Novel Intraglomerular Alternatively Activated Bone Marrow–Derived Macrophages and Mac-1 and PD-L1 in Lupus-Prone NZM2328 Mice

Sung

Dai

et al. 2017

The Journal of Immunology

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Glomerular damage mediated by glomerulus-infiltrating myeloid-derived cells is a key pathogenic event in lupus nephritis (LN)c but the process is poorly understood. Confocal microscopy of kidney sections and flow cytometry analysis of glomerular cells from magnetic-bead purified glomeruli have identified glomerulus-infiltrating leukocyte populations in NZM2328 (NZM) lupus-prone mice with spontaneous chronic glomerulonephritis (cGN) and anti-glomerular basement membrane (GBM)-induced nephritis. The occurrence of a major glomerulus-infiltrating CD11b+F4/80−I-A− macrophage population exhibiting the markers PD-L1, Mac-2, and macrophage mannose receptor (MMR, CD206) and producing Klf4, Il10, Retnla, Tnf, and Il6 mRNA which are known to be expressed by alternatively activated (M2b) macrophages correlated with proteinuria status. In NZM mice with spontaneous LN, glomerular macrophage infiltration is predominant. CD11b+F4/80−I-A− intraglomerular macrophages and PMN are important in inducing GN as anti- CD11b and ICAM-1 mAb inhibited both proteinuria and macrophage and PMN infiltration. The predominant and high expression of PD-L1 by CD11b+F4/80−I-A− glomerular macrophages in kidneys of mice with GN and the inhibition of proteinuria by anti-PD-L1 mAb supported the pathogenic role of these macrophages but not the PD-L1− PMN in GN development and in inducing podocyte damage. In NZM mice with spontaneous cGN and severe proteinuria, few glomerulus-infiltrating PMN were found, leaving macrophages and to a lesser extent DC as the major infiltrating leukocytes. These data taken together support the important pathogenic effect of CD11b+F4/80−I-A− M2b-like glomerulus-infiltrating macrophages in LN and reinforce macrophages as a promising target for GN treatment.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Dependence of Glomerulonephritis Induction on Novel Intraglomerular Alternatively Activated Bone Marrow–Derived Macrophages and Mac-1 and PD-L1 in Lupus-Prone NZM2328 Mice

Sung

Dai

et al. 2017

The Journal of Immunology

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“…stimulus; i.e., they are assumed to be dictated by a dominant etiological stimulus [see the critical discussion in (3,45)]. Central in this context is the ideal role of coherent and interdependent factors/processes like autoimmunity (17,33,(89)(90)(91)(92)(93)(94), target antigens in vivo (5,17,34,35,65,67,77,95,96), complement activation and consumption (97-100), and direct effect on target organs [kidneys (5,(101)(102)(103)(104)(105), skin (106-109), and cerebrum (110)(111)(112)(113)]. Importantly, this ties complexity to causality (85) and is further contemplated in different contexts below.…”

Section: Sle Classification Versus Sle Diagnostic Criteria-an Attempt...mentioning

confidence: 99%

The greatest contribution to medical science is the transformation from studying symptoms to studying their causes—the unrelenting legacy of Robert Koch and Louis Pasteur—and a causality perspective to approach a definition of SLE

Rekvig

2024

Front. Immunol.

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The basic initiative related to this study is derived from the fact that systemic lupus erythematosus (SLE) is a unique and fertile system science subject. We are, however, still far from understanding its nature. It may be fair to indicate that we are spending more time and resources on studying the complexity of classified SLE than studying the validity of classification criteria. This study represents a theoretical analysis of current instinctual1 SLE classification criteria based on “the causality principle.” The discussion has its basis on the radical scientific traditions introduced by Robert Koch and Louis Pasteur. They announced significant changes in our thinking of disease etiology through the implementation of the modern version of “the causality principle.” They influenced all aspects of today’s medical concepts and research: the transformation of medical science from studies of symptoms to study their causes, relevant for monosymptomatic diseases as for syndromes. Their studies focused on bacteria as causes of infectious diseases and on how the immune system adapts to control and prevent contagious spreading. This is the most significant paradigm shift in the modern history of medicine and resulted in radical changes in our view of the immune system. They described acquired post-infection immunity and active immunization by antigen-specific vaccines. The paradigm “transformation” has a great theoretical impact also on current studies of autoimmune diseases like SLE: symptoms and their cause(s). In this study, the evolution of SLE classification and diagnostic criteria is discussed from “the causality principle” perspective, and if contemporary SLE classification criteria are as useful as believed today for SLE research. This skepticism is based on the fact that classification criteria are not selected based on cogent causal strategies. The SLE classification criteria do not harmonize with Koch’s and Pasteur’s causality principle paradigms and not with Witebsky’s Koch-derived postulates for autoimmune and infectious diseases. It is not established whether the classification criteria can separate SLE as a “one disease entity” from “SLE-like non-SLE disorders”—the latter in terms of SLE imitations. This is discussed here in terms of weight, rank, and impact of the classification criteria: Do they all originate from “one basic causal etiology”? Probably not.

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“…It has also been proposed that tissue-resident cells might express receptors for inflammatory cytokines, and respond to these, accentuating local injury; for example, mesangial cells produce IL-6, whereas podocytes express CD86, which may provide costimulation to lymphocytes [140]. Moreover, confocal microscopy has identified the presence of organized lymphoid aggregates, termed tertiary lymphoid organs , in non-lymphoid organs such as the kidneys of patients with lupus nephritis [141]. Furthermore, the use of congenic mice has shown that distinct chromosomal regions determine the development of autoimmunity and chronic kidney damage [142].…”

Section: Tissue Injury In Slementioning

confidence: 99%

Pathogenesis of Human Systemic Lupus Erythematosus: A Cellular Perspective

Moulton

Suárez‐Fueyo

Meidan

et al. 2017

Trends in Molecular Medicine

354

213

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Systemic lupus erythematosus (SLE) is a chronic autoimmune disease affecting multiple organs. A complex interaction of genetics, environment, and hormones leads to immune dysregulation and breakdown of tolerance to self-antigens, resulting in autoantibody production, inflammation, and destruction of end-organs. Emerging evidence on the role of these factors has increased our knowledge of this complex disease, guiding therapeutic strategies and identifying putative biomarkers. Recent findings include the characterization of genetic/epigenetic factors linked to SLE, as well as cellular effectors. Novel observations have provided an improved understanding of the contribution of tissue-specific factors and associated damage, T and B lymphocytes, as well as innate immune cell subsets and their corresponding abnormalities. The intricate web of involved factors and pathways dictates the adoption of tailored therapeutic approaches to conquer this disease.

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Pathogenesis of proliferative lupus nephritis from a historical and personal perspective

Cited by 10 publications

References 29 publications

Dependence of Glomerulonephritis Induction on Novel Intraglomerular Alternatively Activated Bone Marrow–Derived Macrophages and Mac-1 and PD-L1 in Lupus-Prone NZM2328 Mice

Dependence of Glomerulonephritis Induction on Novel Intraglomerular Alternatively Activated Bone Marrow–Derived Macrophages and Mac-1 and PD-L1 in Lupus-Prone NZM2328 Mice

The greatest contribution to medical science is the transformation from studying symptoms to studying their causes—the unrelenting legacy of Robert Koch and Louis Pasteur—and a causality perspective to approach a definition of SLE

Pathogenesis of Human Systemic Lupus Erythematosus: A Cellular Perspective

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