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Article: Lupus autoantibodies 101: one size does not fit all; however, specificity influences pathogenicity.

Madaio, M P

2003 Volume 131, Issue 3, Page(s) 396–397

MeSH term(s)	Animals ; Antibody Specificity ; Autoantibodies/immunology ; Disease Susceptibility/immunology ; Humans ; Lupus Erythematosus, Systemic/immunology ; Neutrophils/immunology
Chemical Substances	Autoantibodies
Language	English
Publishing date	2003-03
Publishing country	England
Document type	Editorial
ZDB-ID	218531-3
ISSN	1365-2249 ; 0009-9104 ; 0964-2536
ISSN (online)	1365-2249
ISSN	0009-9104 ; 0964-2536
DOI	10.1046/j.1365-2249.2003.02112.x
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Article ; Online: Major peptide autoepitopes for nucleosome-specific T cells of human lupus.

Madaio, M P

American journal of kidney diseases : the official journal of the National Kidney Foundation

2000 Volume 35, Issue 5, Page(s) 992–996

MeSH term(s)	Epitopes, T-Lymphocyte/immunology ; Humans ; Lupus Erythematosus, Systemic/immunology ; Nucleosomes/immunology
Chemical Substances	Epitopes, T-Lymphocyte ; Nucleosomes
Language	English
Publishing date	2000-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	604539-x
ISSN	1523-6838 ; 0272-6386
ISSN (online)	1523-6838
ISSN	0272-6386
DOI	10.1016/s0272-6386(00)70277-0
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Zs.A 1669: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article: The role of autoantibodies in the pathogenesis of lupus nephritis.

Madaio, M P

Seminars in nephrology

1999 Volume 19, Issue 1, Page(s) 48–56

Abstract: Despite intensive research over the past three decades, the events leading to pathogenic autoantibody production and immune deposit formation in individuals with systemic lupus erythematosus continues to be debated. The controversy is fueled by the ... ...

Abstract	Despite intensive research over the past three decades, the events leading to pathogenic autoantibody production and immune deposit formation in individuals with systemic lupus erythematosus continues to be debated. The controversy is fueled by the clinical observations that individual patients with lupus have variable expression of disease, and that it is often difficult to completely distinguish the events involved in the initiation of nephritis from the processes leading to progressive disease and organ failure. This review focuses on the mechanisms of immune deposition in individuals with lupus nephritis. Recent evidence derived from both analysis of spontaneously occurring animal models of lupus nephritis and human lupus nephritis suggests that direct binding of autoantibodies to glomerular antigens is an important mechanism in lupus and other immune complex nephritides. In situ deposition of circulating autoantigens and autoantibodies also may play a role. These findings, taken together with observations from analysis of other autoimmune diseases, suggest that autoantigen ligation by autoantibodies may contribute to the inflammatory/fibrogenic response through either direct stimulation of cells or interruption of cell-cell or cell matrix interactions. The nature of these type of interactions in individual patients therefore may have disease-modulating effects. For example, the predominant autoantibody response likely influences the glomerular response to immune deposition and the ensuing inflammation. The evidence for, and implications of, this hypothesis are discussed.
MeSH term(s)	Animals ; Antibody Specificity ; Antigen-Antibody Complex/immunology ; Antigens, Surface/immunology ; Autoantibodies/immunology ; Autoimmunity/immunology ; Binding Sites ; Humans ; Lupus Nephritis/immunology
Chemical Substances	Antigen-Antibody Complex ; Antigens, Surface ; Autoantibodies
Language	English
Publishing date	1999-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	604652-6
ISSN	1558-4488 ; 0270-9295
ISSN (online)	1558-4488
ISSN	0270-9295
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Article: B cells and autoantibodies in the pathogenesis of lupus nephritis.

Madaio, M P

Immunologic research

1998 Volume 17, Issue 1-2, Page(s) 123–132

Abstract: Although autoantibodies and autoantibody-producing B cells are crucial for the initiation of lupus nephritis, their precise role in the development of the nephritic lesions is incompletely understood. This article summarizes the results of recent work in ...

Abstract	Although autoantibodies and autoantibody-producing B cells are crucial for the initiation of lupus nephritis, their precise role in the development of the nephritic lesions is incompletely understood. This article summarizes the results of recent work in our laboratory related to this area. They indicate that not all autoantibodies are pathogenic. Furthermore, among the pathogenic subset, individual immunoglobulins produce clearly distinguishable immune deposit patterns in specific glomerular locations and this is associated with different disease profiles (i.e., inflammation, proteinuria). The variation in immune deposit formation induced by the individual autoantibodies are reminiscent of the different lesions in lupus patients, and they appear to be related to differences in the reactivity of autoantibodies with specific glomerular antigens. Thus, it appears that the predominant interaction in a given individual influences the morphologic and clinical expression of disease. Autoantibody-producing B cells also influence the activation of autoreactive T cells that infiltrate the kidney to produce vasculitis and interstitial nephritis, and the potential mechanisms responsible for this phenomenon are discussed.
MeSH term(s)	Animals ; Autoantibodies/immunology ; B-Lymphocytes/immunology ; Humans ; Lupus Nephritis/immunology ; Lymphocyte Cooperation ; T-Lymphocytes/immunology
Chemical Substances	Autoantibodies
Language	English
Publishing date	1998
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	632857-x
ISSN	1559-0755 ; 0257-277X
ISSN (online)	1559-0755
ISSN	0257-277X
DOI	10.1007/BF02786437
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Article ; Online: Diagnosis and treatment of nephrotic syndrome.

Verma, S P / Madaio, M P

Expert opinion on investigational drugs

2005 Volume 8, Issue 6, Page(s) 787–796

Abstract: Prompt diagnosis is essential in the planning of effective treatment for the underlying diseases responsible for nephrotic syndrome. In this review, the typical clinical and laboratory features that facilitate diagnosis of these disorders are discussed. ... ...

Abstract	Prompt diagnosis is essential in the planning of effective treatment for the underlying diseases responsible for nephrotic syndrome. In this review, the typical clinical and laboratory features that facilitate diagnosis of these disorders are discussed. The distinction between systemic diseases, involving the kidney, and primary glomerular diseases is emphasised. These clinical and pathological distinctions influence prognosis, and form the basis of therapy to treat the underlying disorders. Our discussion focuses on diagnosis and specific treatment of these diseases, as well as therapy of the clinical consequences of nephrotic syndrome per se.
Language	English
Publishing date	2005-06-07
Publishing country	England
Document type	Journal Article
ZDB-ID	1182884-5
ISSN	1744-7658 ; 0967-8298 ; 1354-3784
ISSN (online)	1744-7658
ISSN	0967-8298 ; 1354-3784
DOI	10.1517/13543784.8.6.787
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Article: Pathogenic autoantibodies in lupus nephritis.

Waldman, M / Madaio, M P

Lupus

2005 Volume 14, Issue 1, Page(s) 19–24

Abstract: Lupus nephritis is a major complication of systemic lupus erythematosus (SLE) and is associated with a high rate of morbidity and mortality. While many different immunologic and nonimmunologic factors contribute to disease expression in lupus nephritis, ... ...

Abstract	Lupus nephritis is a major complication of systemic lupus erythematosus (SLE) and is associated with a high rate of morbidity and mortality. While many different immunologic and nonimmunologic factors contribute to disease expression in lupus nephritis, a large body of evidence suggests that the production of anti-DNA antibodies and the formation of glomerular immune deposits are important initial events in the pathogenesis of the disease. This review will summarize our current understanding of the differences between pathogenic and nonpathogenic autoantibodies, the mechanisms by which these autoantibodies induce renal injury and the effector mechanisms which are subsequently activated by the deposited autoantibodies that ultimately lead to the expression of the different lupus lesions.
MeSH term(s)	Antibodies, Antinuclear/immunology ; Autoantibodies/immunology ; Humans ; Lupus Nephritis/immunology ; Lupus Nephritis/physiopathology
Chemical Substances	Antibodies, Antinuclear ; Autoantibodies
Language	English
Publishing date	2005
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	1154407-7
ISSN	0961-2033
ISSN	0961-2033
DOI	10.1191/0961203305lu2054oa
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Article ; Online: SARS-CoV-2 Reinfection in a Liver Transplant Recipient.

Tomkins-Tinch, Christopher H / Daly, Jennifer S / Gladden-Young, Adrianne / Theodoropoulos, Nicole M / Madaio, Michael P / Yu, Neng / Vanguri, Vijay K / Siddle, Katherine J / Adams, Gordon / Krasilnikova, Lydia A / Movahedi, Babak / Bozorgzadeh, Adel / Simin, Karl / Lemieux, Jacob E / Luban, Jeremy / Park, Daniel J / MacInnis, Bronwyn L / Sabeti, Pardis C / Levitz, Stuart M

Annals of internal medicine

2021 Volume 174, Issue 8, Page(s) 1178–1180

MeSH term(s)	COVID-19/diagnosis ; COVID-19/virology ; COVID-19 Nucleic Acid Testing ; Humans ; Immunocompromised Host ; Immunosuppressive Agents ; Liver Transplantation ; Male ; Middle Aged ; Mycophenolic Acid/therapeutic use ; Phylogeny ; Reinfection ; SARS-CoV-2/genetics ; Tacrolimus/therapeutic use
Chemical Substances	Immunosuppressive Agents ; Mycophenolic Acid (HU9DX48N0T) ; Tacrolimus (WM0HAQ4WNM)
Language	English
Publishing date	2021-04-20
Publishing country	United States
Document type	Case Reports ; Letter ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	336-0
ISSN	1539-3704 ; 0003-4819
ISSN (online)	1539-3704
ISSN	0003-4819
DOI	10.7326/L21-0108
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Article ; Online: Human anti-α3(IV)NC1 antibody drug conjugates target glomeruli to resolve nephritis.

Kvirkvelia, Nino / McMenamin, Malgorzata / Gutierrez, Vanessa Iris / Lasareishvili, Besarion / Madaio, Michael P

American journal of physiology. Renal physiology

2015 Volume 309, Issue 8, Page(s) F680–4

Abstract: Current therapies to limit kidney disease progression lack specificity and often have systemic toxicity. To approach this problem, we postulated that a human monoclonal antibody (F1.1), directed against the noncollagenous-1 domain (NC1) of α3(IV) ... ...

Abstract	Current therapies to limit kidney disease progression lack specificity and often have systemic toxicity. To approach this problem, we postulated that a human monoclonal antibody (F1.1), directed against the noncollagenous-1 domain (NC1) of α3(IV) collagen that localizes in glomeruli, could serve as a vehicle for targeted drug delivery. Given enhanced exposure of the NC1 domain of α3(IV) during glomerular diseases, with limited epitope expression in other organs, α3(IV)NC1 provides an ideal target for delivery of disease-modifying agents. As a potential disease-modifying agent, we initially took advantage of recent observations that PGE2 promoted recovery after established injury during the course of nephrotoxic nephritis. To address the general applicability of the approach, the efficacy of glomerular delivery of dexamethasone was also examined. To achieve glomerular targeted therapy, PGE2 and dexamethasone were coupled to F1.1. After confirmation of the composition and activity of the conjugates, both glomerular localization and the capacity of the conjugates to modify disease were evaluated. After injection into mice with established nephritis, resolution of disease was enhanced with both agents, with normalization of histology and improved blood urea nitrogen levels in conjugate-treated mice compared with untreated mice. The results provide a novel means of targeting glomeruli during nephritis, irrespective of cause, by providing efficient drug delivery, with the potential of limiting systemic effects.
MeSH term(s)	Animals ; Anti-Glomerular Basement Membrane Disease/chemically induced ; Anti-Glomerular Basement Membrane Disease/drug therapy ; Anti-Inflammatory Agents/therapeutic use ; Antibodies, Monoclonal/therapeutic use ; Autoantigens/immunology ; Blood Urea Nitrogen ; Cell Line ; Collagen Type IV/immunology ; Dexamethasone/analogs & derivatives ; Dexamethasone/therapeutic use ; Dinoprostone/analogs & derivatives ; Dinoprostone/therapeutic use ; Drug Delivery Systems ; Female ; Hepatocytes ; Humans ; Immunoconjugates/therapeutic use ; Kidney Glomerulus/drug effects ; Mice ; Mice, Inbred C57BL ; Nephritis/drug therapy ; Nephritis/immunology ; Podocytes/drug effects ; Sheep
Chemical Substances	Anti-Inflammatory Agents ; Antibodies, Monoclonal ; Autoantigens ; Collagen Type IV ; Immunoconjugates ; type IV collagen alpha3 chain ; Dexamethasone (7S5I7G3JQL) ; Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2015-10-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00289.2015
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Article ; Online: Best Practices for Physician-Scientist Training Programs: Recommendations from the Alliance for Academic Internal Medicine.

Blanchard, Melvin / Burton, M Caroline / Geraci, Mark W / Madaio, Michael P / Marsh, James D / Proweller, Aaron / Rockey, Don C / Salata, Robert A / Tan, Winston / Williams, Christopher S / Zaidi, Mone / Todd, Robert F

The American journal of medicine

2018 Volume 131, Issue 5, Page(s) 578–584

MeSH term(s)	Biomedical Research/education ; Curriculum ; Education, Medical, Graduate/organization & administration ; Humans ; Internship and Residency ; Mentoring ; Research Support as Topic/statistics & numerical data ; United States
Language	English
Publishing date	2018-02-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80015-6
ISSN	1555-7162 ; 1873-2178 ; 0002-9343 ; 1548-2766
ISSN (online)	1555-7162 ; 1873-2178
ISSN	0002-9343 ; 1548-2766
DOI	10.1016/j.amjmed.2018.01.015
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Article ; Online: Kidney-targeted inhibition of protein kinase C-α ameliorates nephrotoxic nephritis with restoration of mitochondrial dysfunction.

Kvirkvelia, Nino / McMenamin, Malgorzata / Warren, Marie / Jadeja, Ravirajsinh N / Kodeboyina, Sai Karthik / Sharma, Ashok / Zhi, Wenbo / O'Connor, Paul M / Raju, Raghavan / Lucas, Rudolf / Madaio, Michael P

Kidney international

2018 Volume 94, Issue 2, Page(s) 280–291

Abstract: To investigate the role of protein kinase C-α (PKC-α) in glomerulonephritis, the capacity of PKC-α inhibition to reverse the course of established nephrotoxic nephritis (NTN) was evaluated. Nephritis was induced by a single injection of nephrotoxic serum ...

Abstract	To investigate the role of protein kinase C-α (PKC-α) in glomerulonephritis, the capacity of PKC-α inhibition to reverse the course of established nephrotoxic nephritis (NTN) was evaluated. Nephritis was induced by a single injection of nephrotoxic serum and after its onset, a PKC-α inhibitor was administered either systemically or by targeted glomerular delivery. By day seven, all mice with NTN had severe nephritis, whereas mice that received PKC-α inhibitors in either form had minimal evidence of disease. To further understand the underlying mechanism, label-free shotgun proteomic analysis of the kidney cortexes were performed, using quantitative mass spectrometry. Ingenuity pathway analysis revealed 157 differentially expressed proteins and mitochondrial dysfunction as the most modulated pathway. Functional protein groups most affected by NTN were mitochondrial proteins associated with respiratory processes. These proteins were down-regulated in the mice with NTN, while their expression was restored with PKC-α inhibition. This suggests a role for proteins that regulate oxidative phosphorylation in recovery. In cultured glomerular endothelial cells, nephrotoxic serum caused a decrease in mitochondrial respiration and membrane potential, mitochondrial morphologic changes and an increase in glycolytic lactic acid production; all normalized by PKC-α inhibition. Thus, PKC-α has a critical role in NTN progression, and the results implicate mitochondrial processes through restoring oxidative phosphorylation, as an essential mechanism underlying recovery. Importantly, our study provides additional support for targeted therapy to glomeruli to reverse the course of progressive disease.
MeSH term(s)	Animals ; Antibodies, Monoclonal/immunology ; Autoantigens/immunology ; Collagen Type IV/immunology ; Disease Models, Animal ; Drug Delivery Systems/methods ; Female ; Glomerulonephritis/drug therapy ; Glomerulonephritis/immunology ; Glomerulonephritis/pathology ; Humans ; Hybridomas ; Immune Sera/administration & dosage ; Immune Sera/immunology ; Immunoglobulin Fragments/immunology ; Immunoglobulin G/immunology ; Kidney Glomerulus/drug effects ; Kidney Glomerulus/immunology ; Kidney Glomerulus/pathology ; Mice ; Mice, Inbred C57BL ; Mitochondria/drug effects ; Mitochondria/immunology ; Mitochondria/metabolism ; Oxidative Phosphorylation/drug effects ; Protein Kinase C-alpha/antagonists & inhibitors ; Protein Kinase C-alpha/immunology ; Protein Kinase C-alpha/metabolism ; Protein Kinase Inhibitors/immunology ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Treatment Outcome
Chemical Substances	Antibodies, Monoclonal ; Autoantigens ; Collagen Type IV ; Immune Sera ; Immunoglobulin Fragments ; Immunoglobulin G ; Protein Kinase Inhibitors ; type IV collagen alpha3 chain ; Prkca protein, mouse (EC 2.7.11.13) ; Protein Kinase C-alpha (EC 2.7.11.13)
Language	English
Publishing date	2018-05-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2018.01.032
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