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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: 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: Extracellular DNA traps in a ctenophore demonstrate immune cell behaviors in a non-bilaterian.

Vandepas, Lauren E / Stefani, Caroline / Domeier, Phillip P / Traylor-Knowles, Nikki / Goetz, Frederick W / Browne, William E / Lacy-Hulbert, Adam

Nature communications

2024 Volume 15, Issue 1, Page(s) 2990

Abstract: The formation of extracellular DNA traps (ETosis) is a first response mechanism by specific immune cells following exposure to microbes. Initially characterized in vertebrate neutrophils, cells capable of ETosis have been discovered recently in diverse ... ...

Abstract	The formation of extracellular DNA traps (ETosis) is a first response mechanism by specific immune cells following exposure to microbes. Initially characterized in vertebrate neutrophils, cells capable of ETosis have been discovered recently in diverse non-vertebrate taxa. To assess the conservation of ETosis between evolutionarily distant non-vertebrate phyla, we observed and quantified ETosis using the model ctenophore Mnemiopsis leidyi and the oyster Crassostrea gigas. Here we report that ctenophores - thought to have diverged very early from the metazoan stem lineage - possess immune-like cells capable of phagocytosis and ETosis. We demonstrate that both Mnemiopsis and Crassostrea immune cells undergo ETosis after exposure to diverse microbes and chemical agents that stimulate ion flux. We thus propose that ETosis is an evolutionarily conserved metazoan defense against pathogens.
MeSH term(s)	Animals ; Ctenophora/genetics ; Extracellular Traps ; Neutrophils
Language	English
Publishing date	2024-04-06
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-024-46807-6
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Article ; Online: Basophils and Eosinophils in Nematode Infections.

Obata-Ninomiya, Kazushige / Domeier, Phillip P / Ziegler, Steven F

Frontiers in immunology

2020 Volume 11, Page(s) 583824

Abstract: Helminths remain one of the most prolific pathogens in the world. Following infection helminths interact with various epithelial cell surfaces, including skin, lung, and gut. Recent works have shown that epithelial cells produce a series of cytokines ... ...

Abstract	Helminths remain one of the most prolific pathogens in the world. Following infection helminths interact with various epithelial cell surfaces, including skin, lung, and gut. Recent works have shown that epithelial cells produce a series of cytokines such as TSLP, IL-33, and IL-25 that lead to the induction of innate and acquired type 2 immune responses, which we named Type 2 epithelial cytokines. Although basophils and eosinophils are relatively rare granulocytes under normal conditions (0.5% and 5% in peripheral blood, respectively), both are found with increased frequency in type 2 immunity, including allergy and helminth infections. Recent reports showed that basophils and eosinophils not only express effector functions in type 2 immune reactions, but also manipulate the response toward helminths. Furthermore, basophils and eosinophils play non-redundant roles in distinct responses against various nematodes, providing the potential to intervene at different stages of nematode infection. These findings would be helpful to establish vaccination or therapeutic drugs against nematode infections.
MeSH term(s)	Animals ; Basophils/immunology ; Eosinophils/immunology ; Helminths/immunology ; Humans ; Immunity/immunology ; Nematode Infections/immunology
Language	English
Publishing date	2020-11-27
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.2020.583824
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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: STAT3 signaling in B cells controls germinal center zone organization and recycling.

Fike, Adam J / Chodisetti, Sathi Babu / Wright, Nathaniel E / Bricker, Kristen N / Domeier, Phillip P / Maienschein-Cline, Mark / Rosenfeld, Aaron M / Luckenbill, Sara A / Weber, Julia L / Choi, Nicholas M / Luning Prak, Eline T / Mandal, Malay / Clark, Marcus R / Rahman, Ziaur S M

Cell reports

2023 Volume 42, Issue 5, Page(s) 112512

Abstract: Germinal centers (GCs), sites of antibody affinity maturation, are organized into dark (DZ) and light (LZ) zones. Here, we show a B cell-intrinsic role for signal transducer and activator of transcription 3 (STAT3) in GC DZ and LZ organization. Altered ... ...

Abstract	Germinal centers (GCs), sites of antibody affinity maturation, are organized into dark (DZ) and light (LZ) zones. Here, we show a B cell-intrinsic role for signal transducer and activator of transcription 3 (STAT3) in GC DZ and LZ organization. Altered zonal organization of STAT3-deficient GCs dampens development of long-lived plasma cells (LL-PCs) but increases memory B cells (MBCs). In an abundant antigenic environment, achieved here by prime-boost immunization, STAT3 is not required for GC initiation, maintenance, or proliferation but is important for sustaining GC zonal organization by regulating GC B cell recycling. Th cell-derived signals drive STAT3 tyrosine 705 and serine 727 phosphorylation in LZ B cells, regulating their recycling into the DZ. RNA sequencing (RNA-seq) and chromatin immunoprecipitation sequencing (ChIP-seq) analyses identified STAT3 regulated genes that are critical for LZ cell recycling and transiting through DZ proliferation and differentiation phases. Thus, STAT3 signaling in B cells controls GC zone organization and recycling, and GC egress of PCs, but negatively regulates MBC output.
MeSH term(s)	STAT3 Transcription Factor ; B-Lymphocytes ; Germinal Center ; Plasma Cells ; Signal Transduction
Chemical Substances	STAT3 Transcription Factor
Language	English
Publishing date	2023-05-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2023.112512
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Article ; Online: TLR7 Negatively Regulates B10 Cells Predominantly in an IFNγ Signaling Dependent Manner.

Chodisetti, Sathi Babu / Fike, Adam J / Domeier, Phillip P / Choi, Nicholas M / Soni, Chetna / Rahman, Ziaur S M

Frontiers in immunology

2020 Volume 11, Page(s) 1632

Abstract: IL-10 producing B cells (B10 cells) play an important immunoregulatory role in various autoimmune and infection conditions. However, the factors that regulate their development and maintenance are incompletely understood. Recently, we and others have ... ...

Abstract	IL-10 producing B cells (B10 cells) play an important immunoregulatory role in various autoimmune and infection conditions. However, the factors that regulate their development and maintenance are incompletely understood. Recently, we and others have established a requirement for TLR7 in promoting autoimmune antibody forming cell (AFC) and germinal center (GC) responses. Here we report an important additional role of TLR7 in the negative regulation of B10 cell development. TLR7 overexpression or overstimulation promoted the reduction of B10 cells whereas TLR7 deficiency rescued these cells in both non-autoimmune and autoimmune-prone mice. TLR7 expression was further inversely correlated with B cell-dependent IL-10 production and its inhibition of CD4 T cell proliferation and IFNγ production in an
MeSH term(s)	Animals ; Autoimmune Diseases/etiology ; Autoimmune Diseases/metabolism ; Autoimmunity ; B-Lymphocyte Subsets/immunology ; B-Lymphocyte Subsets/metabolism ; Biomarkers ; Disease Models, Animal ; Immunomodulation/genetics ; Immunophenotyping ; Interferon-gamma/genetics ; Interferon-gamma/metabolism ; Interleukin-10/biosynthesis ; Lymphocyte Activation/genetics ; Lymphocyte Activation/immunology ; Lymphocyte Count ; Mice ; Mice, Transgenic ; Signal Transduction ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism ; Toll-Like Receptor 7/metabolism
Chemical Substances	Biomarkers ; Toll-Like Receptor 7 ; Interleukin-10 (130068-27-8) ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2020-07-28
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.01632
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Article ; Online: Context-Dependent miR-21 Regulation of TLR7-Mediated Autoimmune and Foreign Antigen-Driven Antibody-Forming Cell and Germinal Center Responses.

Schell, Stephanie L / Bricker, Kristen N / Fike, Adam J / Chodisetti, Sathi Babu / Domeier, Phillip P / Choi, Nicholas M / Fasnacht, Melinda J / Luckenbill, Sara A / Ziegler, Steven F / Rahman, Ziaur S M

Journal of immunology (Baltimore, Md. : 1950)

2021 Volume 206, Issue 12, Page(s) 2803–2818

Abstract: MicroRNAs (miRNAs) are involved in healthy B cell responses and the loss of tolerance in systemic lupus erythematosus (SLE), although the role of many miRNAs remains poorly understood. Dampening miR-21 activity was previously shown to reduce splenomegaly ...

Abstract	MicroRNAs (miRNAs) are involved in healthy B cell responses and the loss of tolerance in systemic lupus erythematosus (SLE), although the role of many miRNAs remains poorly understood. Dampening miR-21 activity was previously shown to reduce splenomegaly and blood urea nitrogen levels in SLE-prone mice, but the detailed cellular responses and mechanism of action remains unexplored. In this study, using the TLR7 agonist, imiquimod-induced SLE model, we observed that loss of miR-21 in
MeSH term(s)	Animals ; Antibody Formation/immunology ; Antigens/immunology ; Autoimmunity/immunology ; Female ; Male ; Membrane Glycoproteins/immunology ; Mice ; Mice, Knockout ; MicroRNAs/immunology ; Toll-Like Receptor 7/immunology
Chemical Substances	Antigens ; MIRN21 microRNA, mouse ; Membrane Glycoproteins ; MicroRNAs ; Tlr7 protein, mouse ; Toll-Like Receptor 7
Language	English
Publishing date	2021-05-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
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.2001039
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Article ; Online: B-Cell-Intrinsic Type 1 Interferon Signaling Is Crucial for Loss of Tolerance and the Development of Autoreactive B Cells.

Domeier, Phillip P / Chodisetti, Sathi Babu / Schell, Stephanie L / Kawasawa, Yuka Imamura / Fasnacht, Melinda J / Soni, Chetna / Rahman, Ziaur S M

Cell reports

2018 Volume 24, Issue 2, Page(s) 406–418

Abstract: Type 1 interferon (T1IFN) signaling promotes inflammation and lupus pathology, but its role in autoreactive B cell development in the antibody-forming cell (AFC) and germinal center (GC) pathways is unclear. Using a lupus model that allows for focused ... ...

Abstract	Type 1 interferon (T1IFN) signaling promotes inflammation and lupus pathology, but its role in autoreactive B cell development in the antibody-forming cell (AFC) and germinal center (GC) pathways is unclear. Using a lupus model that allows for focused study of the AFC and GC responses, we show that T1IFN signaling is crucial for autoreactive B cell development in the AFC and GC pathways. Through bone marrow chimeras, DNA-reactive B cell transfer, and GC-specific Cre mice, we confirm that IFNαR signaling in B cells promotes autoreactive B cell development into both pathways. Transcriptomic analysis reveals gene expression alterations in multiple signaling pathways in non-GC and GC B cells in the absence of IFNαR. Finally, we find that T1IFN signaling promotes autoreactive B cell development in the AFC and GC pathways by regulating BCR signaling. These data suggest value for anti-IFNαR therapy in individuals with elevated T1IFN activity before clinical disease onset.
MeSH term(s)	Animals ; Antibodies, Antinuclear/metabolism ; Antibody Affinity ; Antibody Formation ; Antigens/metabolism ; Autoantibodies/biosynthesis ; B-Lymphocytes/immunology ; DNA/metabolism ; Female ; Germinal Center/metabolism ; Immune Tolerance ; Immunization ; Interferon Type I/metabolism ; Mice, Inbred C57BL ; Receptor, Interferon alpha-beta/metabolism ; Signal Transduction ; Transcriptome/genetics
Chemical Substances	Antibodies, Antinuclear ; Antigens ; Autoantibodies ; Ifnar1 protein, mouse ; Interferon Type I ; Receptor, Interferon alpha-beta (156986-95-7) ; DNA (9007-49-2)
Language	English
Publishing date	2018-07-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2018.06.046
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Article ; Online: Type II but Not Type I IFN Signaling Is Indispensable for TLR7-Promoted Development of Autoreactive B Cells and Systemic Autoimmunity.

Chodisetti, Sathi Babu / Fike, Adam J / Domeier, Phillip P / Singh, Harinder / Choi, Nicholas M / Corradetti, Chelsea / Kawasawa, Yuka Imamura / Cooper, Timothy K / Caricchio, Roberto / Rahman, Ziaur S M

Journal of immunology (Baltimore, Md. : 1950)

2020 Volume 204, Issue 4, Page(s) 796–809

Abstract: TLR7 is associated with development of systemic lupus erythematosus (SLE), but the underlying mechanisms are incompletely understood. Although TLRs are known to activate type I IFN (T1IFN) signaling, the role of T1IFN and IFN-γ signaling in differential ... ...

Abstract	TLR7 is associated with development of systemic lupus erythematosus (SLE), but the underlying mechanisms are incompletely understood. Although TLRs are known to activate type I IFN (T1IFN) signaling, the role of T1IFN and IFN-γ signaling in differential regulation of TLR7-mediated Ab-forming cell (AFC) and germinal center (GC) responses, and SLE development has never been directly investigated. Using TLR7-induced and TLR7 overexpression models of SLE, we report in this study a previously unrecognized indispensable role of TLR7-induced IFN-γ signaling in promoting AFC and GC responses, leading to autoreactive B cell and SLE development. T1IFN signaling in contrast, only modestly contributed to autoimmune responses and the disease process in these mice. TLR7 ligand imiquimod treated IFN-γ reporter mice show that CD4
MeSH term(s)	Animals ; Autoimmunity/immunology ; B-Lymphocytes/immunology ; Germinal Center/immunology ; Interferon Type I ; Interferon-gamma/immunology ; Lupus Erythematosus, Systemic/immunology ; Lymphocyte Activation/immunology ; Membrane Glycoproteins/immunology ; Mice ; Signal Transduction/immunology ; Toll-Like Receptor 7/immunology
Chemical Substances	IFNG protein, mouse ; Interferon Type I ; Membrane Glycoproteins ; Tlr7 protein, mouse ; Toll-Like Receptor 7 ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2020-01-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
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.1901175
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