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Article ; Online: Lupus Interference With B Cell Tolerance Across the Developmental Continuum.

Pemberton, Sarah E / Jackson, Shaun W

Arthritis & rheumatology (Hoboken, N.J.)

2023 Volume 75, Issue 9, Page(s) 1503–1505

MeSH term(s)	Humans ; B-Lymphocytes ; Immune Tolerance ; Lupus Erythematosus, Systemic
Language	English
Publishing date	2023-07-10
Publishing country	United States
Document type	Editorial ; Research Support, N.I.H., Extramural
ZDB-ID	2756371-6
ISSN	2326-5205 ; 2326-5191
ISSN (online)	2326-5205
ISSN	2326-5191
DOI	10.1002/art.42485
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Article ; Online: Resolving a paradox between mouse and man: a genetic link between TLR7 and the pathogenesis of human lupus nephritis.

Jackson, Shaun W / Rovin, Brad H

Kidney international

2023 Volume 103, Issue 5, Page(s) 824–826

MeSH term(s)	Humans ; Antibodies, Antinuclear ; Autoantibodies ; Lupus Nephritis/genetics ; Lupus Nephritis/pathology ; Toll-Like Receptor 7/genetics
Chemical Substances	Antibodies, Antinuclear ; Autoantibodies ; TLR7 protein, human ; Toll-Like Receptor 7
Language	English
Publishing date	2023-04-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2023.01.019
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Zs.A 797: Show issues

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Article ; Online: Lupus nephritis transcriptomics across space and time.

Jackson, Shaun W / Alpers, Charles E

Kidney international

2022 Volume 102, Issue 4, Page(s) 694–696

Abstract: Current immunosuppression regimens for lupus nephritis are incompletely effective, placing patients at risk for poor long-term outcomes. This emphasizes the need to dissect pathogenic mechanisms in lupus nephritis, to inform the development of targeted ... ...

Abstract	Current immunosuppression regimens for lupus nephritis are incompletely effective, placing patients at risk for poor long-term outcomes. This emphasizes the need to dissect pathogenic mechanisms in lupus nephritis, to inform the development of targeted therapies. In this issue of Kidney International, Parikh et al. performed transcriptomic analysis of pretreatment and posttreatment protocol kidney biopsies, segregated into glomerular and tubulointerstitial compartments, to identify candidate molecular pathways distinguishing treatment responders and nonresponders.
MeSH term(s)	Humans ; Kidney/pathology ; Kidney Glomerulus/pathology ; Lupus Nephritis/genetics ; Lupus Nephritis/pathology ; Transcriptome
Language	English
Publishing date	2022-09-21
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2022.06.028
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Zs.A 797: Show issues

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Article ; Online: Regulatory strategies limiting endosomal Toll-like receptor activation in B cells.

Acharya, Mridu / Jackson, Shaun W

Immunological reviews

2022 Volume 307, Issue 1, Page(s) 66–78

Abstract: The recognition of pathogen-associated nucleic acid (NA) promotes effective immunity against invading pathogens. However, endosomal Toll-like receptor (TLR) activation by self-NA also underlies the pathogenesis of systemic autoimmune diseases, such as ... ...

Abstract	The recognition of pathogen-associated nucleic acid (NA) promotes effective immunity against invading pathogens. However, endosomal Toll-like receptor (TLR) activation by self-NA also underlies the pathogenesis of systemic autoimmune diseases, such as systemic lupus erythematosus (SLE). For this reason, the activation thresholds of NA-sensing TLRs must be tightly regulated to balance protective and pathogenic immune responses. In this study, we will provide an overview of the evolutionary mechanisms designed to limit the aberrant activation of endosomal TLRs by self-ligands, focusing on four broad strategies. These include the following: 1) the production of nucleases able to degrade self-DNA and RNA; 2) the cell-specific regulation of endosomal TLR expression; 3) the spatial and temporal control of TLR positioning at a sub-cellular level; and 4) the modulation of downstream TLR signaling cascades. Given the critical role of B cells in lupus pathogenesis, where possible, we will describe evidence for B cell-specific induction of these regulatory mechanisms. We will also highlight our own work showing how modulation of B cell endolysosomal flux tunes NA-sensing TLR activation signals. In the face of inevitable generation of self-NA during normal cellular turnover, these parallel mechanisms are vital to protect against pathogenic inflammation.
MeSH term(s)	B-Lymphocytes/immunology ; Endosomes/metabolism ; Humans ; Lupus Erythematosus, Systemic/immunology ; Signal Transduction ; Toll-Like Receptors/metabolism
Chemical Substances	Toll-Like Receptors
Language	English
Publishing date	2022-01-17
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	391796-4
ISSN	1600-065X ; 0105-2896
ISSN (online)	1600-065X
ISSN	0105-2896
DOI	10.1111/imr.13065
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Article ; Online: Recent advances in immunotherapies for lupus nephritis.

Kaneko, Machi / Jackson, Shaun W

Pediatric nephrology (Berlin, Germany)

2022 Volume 38, Issue 4, Page(s) 1001–1012

Abstract: Childhood-onset systemic lupus erythematosus (SLE) is characterized by increased rates of kidney involvement, termed lupus nephritis. Despite the significant morbidity and mortality associated with this disease, lupus nephritis trials have been plagued ... ...

Abstract	Childhood-onset systemic lupus erythematosus (SLE) is characterized by increased rates of kidney involvement, termed lupus nephritis. Despite the significant morbidity and mortality associated with this disease, lupus nephritis trials have been plagued by repeated failures to meet clinical endpoints. However, improvements in trial design and the development of targeted approaches have begun to yield promising results, including two new FDA-approved lupus nephritis treatments since 2020. These include belimumab, a monoclonal antibody targeting the B cell survival cytokine BAFF (B cell activating factor), and voclosporin, a cyclosporin analog with improved pharmacokinetic characteristics. In this review, we will summarize the data supporting regulatory approval for these agents in lupus nephritis and highlight ongoing clinical trials targeting the diverse immunologic drivers of renal inflammation in SLE. While pediatric patients remain underrepresented in lupus clinical trials, given the increased severity of childhood-onset SLE and need for long-term protection from kidney damage, we anticipate the need for off-label use of these targeted therapies in the pediatric population. Future studies are needed to define optimal patient selection, drug combinations, and treatment duration in pediatric lupus nephritis.
MeSH term(s)	Humans ; Child ; Lupus Nephritis/drug therapy ; Lupus Erythematosus, Systemic ; Antibodies, Monoclonal/therapeutic use ; Cytokines ; Immunotherapy/methods ; Immunosuppressive Agents/therapeutic use
Chemical Substances	Antibodies, Monoclonal ; Cytokines ; Immunosuppressive Agents
Language	English
Publishing date	2022-07-01
Publishing country	Germany
Document type	Review ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	631932-4
ISSN	1432-198X ; 0931-041X
ISSN (online)	1432-198X
ISSN	0931-041X
DOI	10.1007/s00467-022-05670-7
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Zs.A 2196: Show issues

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Article ; Online: B Cells in Systemic Lupus Erythematosus: From Disease Mechanisms to Targeted Therapies.

Canny, Susan P / Jackson, Shaun W

Rheumatic diseases clinics of North America

2021 Volume 47, Issue 3, Page(s) 395–413

Abstract: B cells exert a prominent contribution to the pathogenesis of systemic lupus erythematosus (SLE). Here, we review the immune mechanisms underlying autoreactive B cell activation in SLE, focusing on how B cell receptor and Toll-like receptor signals ... ...

Abstract	B cells exert a prominent contribution to the pathogenesis of systemic lupus erythematosus (SLE). Here, we review the immune mechanisms underlying autoreactive B cell activation in SLE, focusing on how B cell receptor and Toll-like receptor signals integrate to drive breaks in tolerance to nuclear antigens. In addition, we discuss autoantibody-dependent and autoantibody-independent B cell effector functions during lupus pathogenesis. Finally, we address efforts to target B cells therapeutically in human SLE. Despite initial disappointing clinical trials testing B cell depletion in lupus, more recent studies show promise, emphasizing how greater understanding of underlying immune mechanisms can yield clinical benefits.
MeSH term(s)	Autoantibodies ; B-Lymphocytes ; Humans ; Lupus Erythematosus, Systemic/drug therapy
Chemical Substances	Autoantibodies
Language	English
Publishing date	2021-06-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	92118-x
ISSN	1558-3163 ; 0889-857X
ISSN (online)	1558-3163
ISSN	0889-857X
DOI	10.1016/j.rdc.2021.04.006
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Article ; Online: BAFF inhibition in SLE-Is tolerance restored?

Jackson, Shaun W / Davidson, Anne

Immunological reviews

2019 Volume 292, Issue 1, Page(s) 102–119

Abstract: The B cell activating factor (BAFF) inhibitor, belimumab, is the first biologic drug approved for the treatment of SLE, and exhibits modest, but durable, efficacy in decreasing disease flares and organ damage. BAFF and its homolog APRIL are TNF-like ... ...

Abstract	The B cell activating factor (BAFF) inhibitor, belimumab, is the first biologic drug approved for the treatment of SLE, and exhibits modest, but durable, efficacy in decreasing disease flares and organ damage. BAFF and its homolog APRIL are TNF-like cytokines that support the survival and differentiation of B cells at distinct developmental stages. BAFF is a crucial survival factor for transitional and mature B cells that acts as rheostat for the maturation of low-affinity autoreactive cells. In addition, BAFF augments innate B cell responses via complex interactions with the B cell receptor (BCR) and Toll like receptor (TLR) pathways. In this manner, BAFF impacts autoreactive B cell activation via extrafollicular pathways and fine tunes affinity selection within germinal centers (GC). Finally, BAFF and APRIL support plasma cell survival, with differential impacts on IgM- and IgG-producing populations. Therapeutically, BAFF and combined BAFF/APRIL inhibition delays disease onset in diverse murine lupus strains, although responsiveness to BAFF inhibition is model dependent, in keeping with heterogeneity in clinical responses to belimumab treatment in humans. In this review, we discuss the mechanisms whereby BAFF/APRIL signals promote autoreactive B cell activation, discuss whether altered selection accounts for therapeutic benefits of BAFF inhibition, and address whether new insights into BAFF/APRIL family complexity can be exploited to improve human lupus treatments.
MeSH term(s)	Animals ; Antibodies, Monoclonal, Humanized/therapeutic use ; B-Cell Activating Factor/antagonists & inhibitors ; B-Cell Activating Factor/immunology ; B-Cell Activating Factor/metabolism ; Humans ; Immune Tolerance/drug effects ; Immune Tolerance/immunology ; Immunosuppressive Agents/therapeutic use ; Lupus Erythematosus, Systemic/drug therapy ; Lupus Erythematosus, Systemic/immunology ; Lupus Erythematosus, Systemic/metabolism ; Receptors, Antigen, B-Cell/immunology ; Receptors, Antigen, B-Cell/metabolism ; Signal Transduction/drug effects ; Signal Transduction/immunology ; Tumor Necrosis Factor Ligand Superfamily Member 13/immunology ; Tumor Necrosis Factor Ligand Superfamily Member 13/metabolism
Chemical Substances	Antibodies, Monoclonal, Humanized ; B-Cell Activating Factor ; Immunosuppressive Agents ; Receptors, Antigen, B-Cell ; Tumor Necrosis Factor Ligand Superfamily Member 13 ; belimumab (73B0K5S26A)
Language	English
Publishing date	2019-09-28
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	391796-4
ISSN	1600-065X ; 0105-2896
ISSN (online)	1600-065X
ISSN	0105-2896
DOI	10.1111/imr.12810
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Article ; Online: NADPH oxidase exerts a B cell-intrinsic contribution to lupus risk by modulating endosomal TLR signals.

Liu, Shuozhi / Lagos, Jonathan / Shumlak, Natali M / Largent, Andrea D / Lewis, Sebastien T E / Holder, Ursula / Du, Samuel W / Liu, Yifan / Hou, Baidong / Acharya, Mridu / Jackson, Shaun W

The Journal of experimental medicine

2024 Volume 221, Issue 4

Abstract: Genome-wide association studies in systemic lupus erythematosus (SLE) have linked loss-of-function mutations in phagocytic NADPH oxidase complex (NOX2) genes, including NCF1 and NCF2, to disease pathogenesis. The prevailing model holds that reduced NOX2 ... ...

Abstract	Genome-wide association studies in systemic lupus erythematosus (SLE) have linked loss-of-function mutations in phagocytic NADPH oxidase complex (NOX2) genes, including NCF1 and NCF2, to disease pathogenesis. The prevailing model holds that reduced NOX2 activity promotes SLE via defective efferocytosis, the immunologically silent clearance of apoptotic cells. Here, we describe a parallel B cell-intrinsic mechanism contributing to breaks in tolerance. In keeping with an important role for B cell Toll-like receptor (TLR) pathways in lupus pathogenesis, NOX2-deficient B cells exhibit enhanced signaling downstream of endosomal TLRs, increased humoral responses to nucleic acid-containing antigens, and the propensity toward humoral autoimmunity. Mechanistically, TLR-dependent NOX2 activation promotes LC3-mediated maturation of TLR-containing endosomes, resulting in signal termination. CRISPR-mediated disruption of NCF1 confirmed a direct role for NOX2 in regulating endosomal TLR signaling in primary human B cells. Together, these data highlight a new B cell-specific mechanism contributing to autoimmune risk in NCF1 and NCF2 variant carriers.
MeSH term(s)	Humans ; NADPH Oxidases/genetics ; Genome-Wide Association Study ; Autoimmunity/genetics ; Endosomes ; Lupus Erythematosus, Systemic/genetics
Chemical Substances	NADPH Oxidases (EC 1.6.3.-)
Language	English
Publishing date	2024-03-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20230774
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Article ; Online: Dysregulated IFN-γ signals promote autoimmunity in STAT1 gain-of-function syndrome.

Largent, Andrea D / Lambert, Katharina / Chiang, Kristy / Shumlak, Natali / Liggitt, Denny / Oukka, Mohammed / Torgerson, Troy R / Buckner, Jane H / Allenspach, Eric J / Rawlings, David J / Jackson, Shaun W

Science translational medicine

2023 Volume 15, Issue 703, Page(s) eade7028

Abstract: Heterozygous signal transducer and activator of transcription 1 ( ...

Abstract	Heterozygous signal transducer and activator of transcription 1 (
MeSH term(s)	Humans ; Child ; Mice ; Animals ; Autoimmunity/genetics ; Gain of Function Mutation ; Interferon-gamma/metabolism ; Syndrome ; Inflammation ; STAT1 Transcription Factor/genetics ; STAT1 Transcription Factor/metabolism
Chemical Substances	Interferon-gamma (82115-62-6) ; STAT1 Transcription Factor ; STAT1 protein, human
Language	English
Publishing date	2023-07-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2518854-9
ISSN	1946-6242 ; 1946-6234
ISSN (online)	1946-6242
ISSN	1946-6234
DOI	10.1126/scitranslmed.ade7028
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Article ; Online: Cutting Edge: Systemic Autoimmunity in Murine STAT3 Gain-of-Function Syndrome Is Characterized by Effector T Cell Expansion in the Absence of Overt Regulatory T Cell Dysfunction.

Woods, Jonathan / Pemberton, Sarah E / Largent, Andrea D / Chiang, Kristy / Liggitt, Denny / Oukka, Mohamed / Rawlings, David J / Jackson, Shaun W

Journal of immunology (Baltimore, Md. : 1950)

2022 Volume 209, Issue 6, Page(s) 1033–1038

Abstract: Germline gain-of-function mutations in the transcriptional ... ...

Abstract	Germline gain-of-function mutations in the transcriptional factor
MeSH term(s)	Animals ; Autoimmunity ; CD8-Positive T-Lymphocytes/metabolism ; Cell Differentiation ; Gain of Function Mutation ; Gene Knock-In Techniques ; Humans ; Inflammation/pathology ; Mice ; Mice, Transgenic ; STAT3 Transcription Factor/genetics ; T-Lymphocytes, Regulatory ; Th17 Cells
Chemical Substances	STAT3 Transcription Factor ; STAT3 protein, human ; Stat3 protein, mouse
Language	English
Publishing date	2022-08-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.2100920
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