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Article ; Online: B cell- and T cell-intrinsic regulation of germinal centers by thymic stromal lymphopoietin signaling.

Domeier, Phillip P / Rahman, Ziaur S M / Ziegler, Steven F

Science immunology

2023 Volume 8, Issue 79, Page(s) eadd9413

Abstract: Long-lived and high-affinity antibodies are derived from germinal center (GC) activity, but the cytokines that regulate GC function are still being identified. Here, we show that thymic stromal lymphopoietin (TSLP) signaling regulates the GC and the ... ...

Abstract	Long-lived and high-affinity antibodies are derived from germinal center (GC) activity, but the cytokines that regulate GC function are still being identified. Here, we show that thymic stromal lymphopoietin (TSLP) signaling regulates the GC and the magnitude of antigen-specific antibody responses. Both GC B cells and T follicular helper (T
MeSH term(s)	Cytokines ; Germinal Center/metabolism ; Receptors, Cytokine/metabolism ; Signal Transduction ; T-Lymphocytes/metabolism ; Thymic Stromal Lymphopoietin ; B-Lymphocytes/metabolism
Chemical Substances	Cytokines ; Receptors, Cytokine ; Thymic Stromal Lymphopoietin (GT0IL38SP4)
Language	English
Publishing date	2023-01-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	2470-9468
ISSN (online)	2470-9468
DOI	10.1126/sciimmunol.add9413
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Article ; Online: miRNA-Mediated Control of B Cell Responses in Immunity and SLE.

Schell, Stephanie L / Rahman, Ziaur S M

Frontiers in immunology

2021 Volume 12, Page(s) 683710

Abstract: Loss of B cell tolerance is central to autoimmune diseases such as systemic lupus erythematosus (SLE). As such, the mechanisms involved in B cell development, maturation, activation, and function that are aberrantly regulated in SLE are of interest in ... ...

Abstract	Loss of B cell tolerance is central to autoimmune diseases such as systemic lupus erythematosus (SLE). As such, the mechanisms involved in B cell development, maturation, activation, and function that are aberrantly regulated in SLE are of interest in the design of targeted therapeutics. While many factors are involved in the generation and regulation of B cell responses, miRNAs have emerged as critical regulators of these responses within the last decade. To date, miRNA involvement in B cell responses has largely been studied in non-autoimmune, immunization-based systems. However, miRNA profiles have also been strongly associated with SLE in human patients and these molecules have proven critical in both the promotion and regulation of disease in mouse models and in the formation of autoreactive B cell responses. Functionally, miRNAs are small non-coding RNAs that bind to complementary sequences located in target mRNA transcripts to mediate transcript degradation or translational repression, invoking a post-transcriptional level of genetic regulation. Due to their capacity to target a diverse range of transcripts and pathways in different immune cell types and throughout the various stages of development and response, targeting miRNAs is an interesting potential therapeutic avenue. Herein, we focus on what is currently known about miRNA function in both normal and SLE B cell responses, primarily highlighting miRNAs with confirmed functions in mouse models. We also discuss areas that should be addressed in future studies and whether the development of miRNA-centric therapeutics may be a viable alternative for the treatment of SLE.
MeSH term(s)	Animals ; B-Lymphocytes/immunology ; Disease Models, Animal ; Germinal Center/immunology ; Humans ; Immune Tolerance ; Lupus Erythematosus, Systemic/immunology ; Mice ; MicroRNAs/biosynthesis ; MicroRNAs/genetics
Chemical Substances	MicroRNAs
Language	English
Publishing date	2021-05-17
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.683710
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Article ; Online: Regulation of B Cell Responses in SLE by Three Classes of Interferons.

Domeier, Phillip P / Rahman, Ziaur S M

International journal of molecular sciences

2021 Volume 22, Issue 19

Abstract: There are three classes of interferons (type 1, 2, and 3) that can contribute to the development and maintenance of various autoimmune diseases, including systemic lupus erythematosus (SLE). Each class of interferons promotes the generation of ... ...

Abstract	There are three classes of interferons (type 1, 2, and 3) that can contribute to the development and maintenance of various autoimmune diseases, including systemic lupus erythematosus (SLE). Each class of interferons promotes the generation of autoreactive B cells and SLE-associated autoantibodies by distinct signaling mechanisms. SLE patients treated with various type 1 interferon-blocking biologics have diverse outcomes, suggesting that additional environmental and genetic factors may dictate how these cytokines contribute to the development of autoreactive B cells and SLE. Understanding how each class of interferons controls B cell responses in SLE is necessary for developing optimized B cell- and interferon-targeted therapeutics. In this review, we will discuss how each class of interferons differentially promotes the loss of peripheral B cell tolerance and leads to the development of autoreactive B cells, autoantibodies, and SLE.
MeSH term(s)	Animals ; Autoantibodies ; B-Lymphocytes/immunology ; Humans ; Interferons/immunology ; Interferons/metabolism ; Lupus Erythematosus, Systemic ; Signal Transduction
Chemical Substances	Autoantibodies ; Interferons (9008-11-1)
Language	English
Publishing date	2021-09-28
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms221910464
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Article ; Online: The Post-GWAS Era: How to Validate the Contribution of Gene Variants in Lupus.

Fike, Adam J / Elcheva, Irina / Rahman, Ziaur S M

Current rheumatology reports

2019 Volume 21, Issue 1, Page(s) 3

Abstract: Purpose of review: Systemic lupus erythematosus (SLE) is a complex autoimmune disease with strong genetic associations. Here, we provide an update on recent advancements in validating SLE candidate genes and risk variants identified in genome-wide ... ...

Abstract	Purpose of review: Systemic lupus erythematosus (SLE) is a complex autoimmune disease with strong genetic associations. Here, we provide an update on recent advancements in validating SLE candidate genes and risk variants identified in genome-wide association studies (GWAS). Recent findings: A pairing of computational biology with new and emerging techniques has significantly increased our understanding of SLE associated variants. Specifically, generation of mutations within mice and examination of patient samples has been the dominant mechanisms for variant validation. While progress has been made in validating some genes, the number of associated genes is growing with minimal exploration of the effects of individual variants on SLE. This indicates that further examination of SLE risk variants in a cell-type-specific manner is required for better understanding of their contributions to SLE disease mechanisms.
MeSH term(s)	Animals ; Gene Expression Regulation ; Genetic Predisposition to Disease ; Genetic Variation ; Genome-Wide Association Study/methods ; Humans ; Interferon Regulatory Factors/genetics ; Interferon-Induced Helicase, IFIH1/genetics ; Lupus Erythematosus, Systemic/genetics ; Lupus Erythematosus, Systemic/immunology ; Lymphocyte Cooperation/genetics ; Lymphocyte Cooperation/immunology ; Mice ; Polymorphism, Single Nucleotide ; Receptors, Antigen, B-Cell/genetics ; Receptors, Antigen, B-Cell/immunology
Chemical Substances	IRF5 protein, human ; Interferon Regulatory Factors ; Receptors, Antigen, B-Cell ; IFIH1 protein, human (EC 3.6.1.-) ; Interferon-Induced Helicase, IFIH1 (EC 3.6.4.13)
Language	English
Publishing date	2019-01-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2057357-1
ISSN	1534-6307 ; 1523-3774
ISSN (online)	1534-6307
ISSN	1523-3774
DOI	10.1007/s11926-019-0801-5
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Zs.A 5531: Show issues

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Article ; Online: New developments implicating IL-21 in autoimmune disease.

Ren, Heather M / Lukacher, Aron E / Rahman, Ziaur S M / Olsen, Nancy J

Journal of autoimmunity

2021 Volume 122, Page(s) 102689

Abstract: Elevated interleukin (IL)-21 is a common finding in the tissues and/or sera of patients with autoimmune disease. CD4 T cells are the primary producers of IL-21; often the IL-21 producing CD4 T cells will express molecules associated with follicular ... ...

Abstract	Elevated interleukin (IL)-21 is a common finding in the tissues and/or sera of patients with autoimmune disease. CD4 T cells are the primary producers of IL-21; often the IL-21 producing CD4 T cells will express molecules associated with follicular helper cells (T
MeSH term(s)	Animals ; Autoimmune Diseases/blood ; Autoimmune Diseases/immunology ; CD8-Positive T-Lymphocytes/immunology ; Cell Differentiation/immunology ; Disease Models, Animal ; Humans ; Immunologic Memory ; Interleukins/metabolism ; Receptors, Interleukin-21/metabolism ; Signal Transduction/immunology ; T Follicular Helper Cells/immunology ; T Follicular Helper Cells/metabolism
Chemical Substances	Interleukins ; Receptors, Interleukin-21 ; interleukin-21 (MKM3CA6LT1)
Language	English
Publishing date	2021-07-02
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	639452-8
ISSN	1095-9157 ; 0896-8411
ISSN (online)	1095-9157
ISSN	0896-8411
DOI	10.1016/j.jaut.2021.102689
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Zs.A 2368: Show issues

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Article ; Online: The mitochondrial sodium/calcium exchanger NCLX (Slc8b1) in B lymphocytes.

Emrich, Scott M / Yoast, Ryan E / Fike, Adam J / Bricker, Kristen N / Xin, Ping / Zhang, Xuexin / Rahman, Ziaur S M / Trebak, Mohamed

Cell calcium

2022 Volume 108, Page(s) 102667

Abstract: Antigen receptor stimulation triggers cytosolic ... ...

Abstract	Antigen receptor stimulation triggers cytosolic Ca
MeSH term(s)	Animals ; Mice ; B-Lymphocytes/metabolism ; Calcium/metabolism ; Calcium Signaling/physiology ; Mice, Knockout ; Mitochondria/metabolism ; Sodium/metabolism ; Sodium-Calcium Exchanger/metabolism
Chemical Substances	Calcium (SY7Q814VUP) ; Sodium (9NEZ333N27) ; Sodium-Calcium Exchanger ; Slc8b1protein, mouse
Language	English
Publishing date	2022-10-20
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	757687-0
ISSN	1532-1991 ; 0143-4160
ISSN (online)	1532-1991
ISSN	0143-4160
DOI	10.1016/j.ceca.2022.102667
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Article ; Online: Spontaneous germinal centers and autoimmunity.

Domeier, Phillip P / Schell, Stephanie L / Rahman, Ziaur S M

Autoimmunity

2017 Volume 50, Issue 1, Page(s) 4–18

Abstract: Germinal centers (GCs) are dynamic microenvironments that form in the secondary lymphoid organs and generate somatically mutated high-affinity antibodies necessary to establish an effective humoral immune response. Tight regulation of GC responses is ... ...

Abstract	Germinal centers (GCs) are dynamic microenvironments that form in the secondary lymphoid organs and generate somatically mutated high-affinity antibodies necessary to establish an effective humoral immune response. Tight regulation of GC responses is critical for maintaining self-tolerance. GCs can arise in the absence of purposeful immunization or overt infection (called spontaneous GCs, Spt-GCs). In autoimmune-prone mice and patients with autoimmune disease, aberrant regulation of Spt-GCs is thought to promote the development of somatically mutated pathogenic autoantibodies and the subsequent development of autoimmunity. The mechanisms that control the formation of Spt-GCs and promote systemic autoimmune diseases remain an open question and the focus of ongoing studies. Here, we discuss the most current studies on the role of Spt-GCs in autoimmunity.
Language	English
Publishing date	2017-02
Publishing country	England
Document type	Journal Article
ZDB-ID	1025450-x
ISSN	1607-842X ; 0891-6934
ISSN (online)	1607-842X
ISSN	0891-6934
DOI	10.1080/08916934.2017.1280671
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Article ; Online: Impaired clearance of apoptotic cells in germinal centers: implications for loss of B cell tolerance and induction of autoimmunity.

Rahman, Ziaur S M

Immunologic research

2011 Volume 51, Issue 2-3, Page(s) 125–133

Abstract: Germinal centers (GCs) comprise lymphoid microenvironments where antigen-stimulated B cells undergo rapid proliferation and somatic hypermutation (SHM), resulting in the generation of B cells with high affinity for antigen. However, this process also ... ...

Abstract	Germinal centers (GCs) comprise lymphoid microenvironments where antigen-stimulated B cells undergo rapid proliferation and somatic hypermutation (SHM), resulting in the generation of B cells with high affinity for antigen. However, this process also generates B cell clones with low antigen affinity and with the potential for autoreactivity. It has been suggested that GC B cells with low antigen affinity and autoreactivity are eliminated via apoptosis and are rapidly cleared by tingible body macrophages (TBMφs). Inefficient clearance of apoptotic cells (ACs) results in autoimmunity that is thought to be mediated by various intracellular molecules possessing danger-associated molecular patterns (DAMPs), including nuclear self-Ags. DAMPs can be released from ACs undergoing "secondary necrosis" due to a disruption in AC clearance within GCs. This review discusses the role and mechanisms associated with impaired clearance of ACs in GCs in loss of B cell tolerance leading to autoantibody production and the development of autoimmunity.
MeSH term(s)	Animals ; Apoptosis ; Autoimmunity ; B-Lymphocytes/immunology ; Cell Differentiation/immunology ; Germinal Center/immunology ; Humans ; Immune Tolerance ; Macrophages/immunology ; Receptors, Pattern Recognition/immunology
Chemical Substances	Receptors, Pattern Recognition
Language	English
Publishing date	2011-10-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	632857-x
ISSN	1559-0755 ; 0257-277X
ISSN (online)	1559-0755
ISSN	0257-277X
DOI	10.1007/s12026-011-8248-4
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Article ; Online: STAT4 Is Largely Dispensable for Systemic Lupus Erythematosus-like Autoimmune- and Foreign Antigen-Driven Antibody-Forming Cell, Germinal Center, and Follicular Th Cell Responses.

Fike, Adam J / Chodisetti, Sathi Babu / Bricker, Kristen N / Choi, Nicholas M / Chroneos, Zissis C / Kaplan, Mark H / Rahman, Ziaur S M

ImmunoHorizons

2021 Volume 5, Issue 1, Page(s) 2–15

Abstract: Genome-wide association studies identified variants in the transcription ... ...

Abstract	Genome-wide association studies identified variants in the transcription factor
MeSH term(s)	Animals ; Autoantibodies/blood ; Autoantigens/immunology ; Autoimmunity ; B-Lymphocytes/immunology ; Disease Models, Animal ; Genome-Wide Association Study ; Germinal Center/immunology ; Lupus Erythematosus, Systemic/genetics ; Lupus Erythematosus, Systemic/metabolism ; Mice ; Mice, Inbred C57BL ; STAT4 Transcription Factor/genetics ; STAT4 Transcription Factor/metabolism ; T-Lymphocytes, Helper-Inducer/immunology
Chemical Substances	Autoantibodies ; Autoantigens ; STAT4 Transcription Factor ; Stat4 protein, mouse
Language	English
Publishing date	2021-01-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2573-7732
ISSN (online)	2573-7732
DOI	10.4049/immunohorizons.2000111
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Article ; Online: Selenium supplementation suppresses immunological and serological features of lupus in B6.Sle1b mice.

Soni, Chetna / Sinha, Indu / Fasnacht, Melinda J / Olsen, Nancy J / Rahman, Ziaur S M / Sinha, Raghu

Autoimmunity

2019 Volume 52, Issue 2, Page(s) 57–68

Abstract: Systemic lupus erythematosus (SLE) is a debilitating multi-factorial immunological disorder characterized by increased inflammation and development of anti-nuclear autoantibodies. Selenium (Se) is an essential trace element with beneficial anti-cancer ... ...

Abstract	Systemic lupus erythematosus (SLE) is a debilitating multi-factorial immunological disorder characterized by increased inflammation and development of anti-nuclear autoantibodies. Selenium (Se) is an essential trace element with beneficial anti-cancer and anti-inflammatory immunological functions. In our previous proteomics study, analysis of Se-responsive markers in the circulation of Se-supplemented healthy men showed a significant increase in complement proteins. Additionally, Se supplementation prolonged the life span of lupus prone NZB/NZW-F1 mice. To better understand the protective immunological role of Se in SLE pathogenesis, we have investigated the impact of Se on B cells and macrophages using in vitro Se supplementation assays and the B6.Sle1b mouse model of lupus with an oral Se or placebo supplementation regimen. Analysis of Se-treated B6.Sle1b mice showed reduced splenomegaly and splenic cellularity compared to untreated B6. Sle1b mice. A significant reduction in total B cells and notably germinal center (GC) B cell numbers was observed. However, other cell types including T cells, Tregs, DCs and pDCs were unaffected. Consistent with reduced GC B cells there was a significant reduction in autoantibodies to dsDNA and SmRNP of the IgG2b and IgG2c subclass upon Se supplementation. We found that increased Se availability leads to impaired differentiation and maturation of macrophages from mouse bone marrow derived progenitors in vitro. Additionally, Se treatment during in vitro activation of B cells with anti-CD40L and LPS inhibited optimal B cell activation. Overall our data indicate that Se supplementation inhibits activation, differentiation and maturation of B cells and macrophages. Its specific inhibitory effect on B cell activation and GC B cell differentiation could be explored as a potential therapeutic supplement for SLE patients.
MeSH term(s)	Animals ; Antibodies, Antinuclear/immunology ; B-Lymphocytes/immunology ; B-Lymphocytes/pathology ; Disease Models, Animal ; Immunoglobulin G/immunology ; Lupus Erythematosus, Systemic/drug therapy ; Lupus Erythematosus, Systemic/immunology ; Lupus Erythematosus, Systemic/pathology ; Macrophages/immunology ; Macrophages/pathology ; Mice ; Selenium/pharmacology
Chemical Substances	Antibodies, Antinuclear ; Immunoglobulin G ; Selenium (H6241UJ22B)
Language	English
Publishing date	2019-04-22
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1025450-x
ISSN	1607-842X ; 0891-6934
ISSN (online)	1607-842X
ISSN	0891-6934
DOI	10.1080/08916934.2019.1603297
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