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Article ; Online: Autoreactive antibodies control blood glucose by regulating insulin homeostasis.

Amendt, Timm / Allies, Gabriele / Nicolò, Antonella / El Ayoubi, Omar / Young, Marc / Röszer, Tamás / Setz, Corinna S / Warnatz, Klaus / Jumaa, Hassan

Proceedings of the National Academy of Sciences of the United States of America

2022 Volume 119, Issue 6

Abstract: Homeostasis of metabolism by hormone production is crucial for maintaining physiological integrity, as disbalance can cause severe metabolic disorders such as diabetes mellitus. Here, we show that antibody-deficient mice and immunodeficiency patients ... ...

Abstract	Homeostasis of metabolism by hormone production is crucial for maintaining physiological integrity, as disbalance can cause severe metabolic disorders such as diabetes mellitus. Here, we show that antibody-deficient mice and immunodeficiency patients have subphysiological blood glucose concentrations. Restoring blood glucose physiology required total IgG injections and insulin-specific IgG antibodies detected in total IgG preparations and in the serum of healthy individuals. In addition to the insulin-neutralizing anti-insulin IgG, we identified two fractions of anti-insulin IgM in the serum of healthy individuals. These autoreactive IgM fractions differ in their affinity to insulin. Interestingly, the low-affinity IgM fraction (anti-insulin IgM
MeSH term(s)	Animals ; Antibody Affinity/immunology ; Autoantibodies/immunology ; Autoimmune Diseases/immunology ; Blood Glucose/immunology ; Female ; Homeostasis/immunology ; Humans ; Immune Tolerance/immunology ; Immunoglobulin G/immunology ; Immunoglobulin M/immunology ; Insulin/immunology ; Mice ; Mice, Inbred C57BL
Chemical Substances	Autoantibodies ; Blood Glucose ; Immunoglobulin G ; Immunoglobulin M ; Insulin
Language	English
Publishing date	2022-02-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2115695119
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Article ; Online: Primary Immune Responses and Affinity Maturation Are Controlled by IgD.

Amendt, Timm / Ayoubi, Omar El / Linder, Alexandra T / Allies, Gabriele / Young, Marc / Setz, Corinna S / Jumaa, Hassan

Frontiers in immunology

2021 Volume 12, Page(s) 709240

Abstract: Mature B cells co-express IgM and IgD B cell antigen receptors (BCR) on their surface. While IgM BCR expression is already essential at early stages of development, the role of the IgD-class BCR remains unclear as most B cell functions appeared unchanged ...

Abstract	Mature B cells co-express IgM and IgD B cell antigen receptors (BCR) on their surface. While IgM BCR expression is already essential at early stages of development, the role of the IgD-class BCR remains unclear as most B cell functions appeared unchanged in IgD-deficient mice. Here, we show that IgD-deficient mice have an accelerated rate of B cell responsiveness as they activate antibody production within 24h after immunization, whereas wildtype (WT) animals required 3 days to activate primary antibody responses. Strikingly, soluble monovalent antigen suppresses IgG antibody production induced by multivalent antigen in WT mice. In contrast, IgD-deficient mice were not able to modulate IgG responses suggesting that IgD controls the activation rate of B cells and subsequent antibody production by sensing and distinguishing antigen-valences. Using an insulin-derived peptide we tested the role of IgD in autoimmunity. We show that primary autoreactive antibody responses are generated in WT and in IgD-deficient mice. However, insulin-specific autoantibodies were detected earlier and caused more severe symptoms of autoimmune diabetes in IgD-deficient mice as compared to WT mice. The rapid control of autoimmune diabetes in WT animals was associated with the generation of high-affinity IgM that protects insulin from autoimmune degradation. In IgD-deficient mice, however, the generation of high-affinity protective IgM is delayed resulting in prolonged autoimmune diabetes. Our data suggest that IgD is required for the transition from primary, highly autoreactive, to secondary antigen-specific antibody responses generated by affinity maturation.
MeSH term(s)	Animals ; Antibody Affinity ; Antibody Formation ; Autoantigens/immunology ; Autoimmunity ; B-Lymphocytes/immunology ; Female ; Immunoglobulin D/physiology ; Immunoglobulin G/biosynthesis ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Receptors, Antigen, B-Cell/immunology
Chemical Substances	Autoantigens ; Immunoglobulin D ; Immunoglobulin G ; Receptors, Antigen, B-Cell
Language	English
Publishing date	2021-08-09
Publishing country	Switzerland
Document type	Journal Article ; 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.2021.709240
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Article ; Online: PI3K induces B-cell development and regulates B cell identity.

Abdelrasoul, Hend / Werner, Markus / Setz, Corinna S / Okkenhaug, Klaus / Jumaa, Hassan

Scientific reports

2018 Volume 8, Issue 1, Page(s) 1327

Abstract: Phosphoinositide-3 kinase (PI3K) signaling is important for the survival of numerous cell types and class IA of PI3K is specifically required for the development of B cells but not for T cell development. Here, we show that class IA PI3K-mediated signals ...

Abstract	Phosphoinositide-3 kinase (PI3K) signaling is important for the survival of numerous cell types and class IA of PI3K is specifically required for the development of B cells but not for T cell development. Here, we show that class IA PI3K-mediated signals induce the expression of the transcription factor Pax5, which plays a central role in B cell commitment and differentiation by activating the expression of central B cell-specific signaling proteins such as SLP-65 and CD19. Defective class IA PI3K function leads to reduction in Pax5 expression and prevents B cell development beyond the stage expressing the precursor B cell receptor (pre-BCR). Investigating the mechanism of PI3K-induced Pax5 expression revealed that it involves a network of transcription factors including FoxO1 and Irf4 that directly binds to the Pax5 gene. Together, our results suggest that PI3K signaling links survival and differentiation of developing B cells with B cell identity and that decreased PI3K activity in pre-B cells results in reduced Pax5 expression and lineage plasticity.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Antigens, CD19/metabolism ; B-Lymphocytes/cytology ; B-Lymphocytes/metabolism ; Cell Line ; Cell Lineage ; Cells, Cultured ; Forkhead Box Protein O1/metabolism ; Interferon Regulatory Factors/metabolism ; Lymphopoiesis ; Mice ; PAX5 Transcription Factor/metabolism ; Phosphatidylinositol 3-Kinases/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; Antigens, CD19 ; B cell linker protein ; Forkhead Box Protein O1 ; Foxo1 protein, mouse ; Interferon Regulatory Factors ; PAX5 Transcription Factor ; Pax5 protein, mouse ; interferon regulatory factor-4 ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-)
Language	English
Publishing date	2018-01-22
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-19460-5
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Article ; Online: PI3K induces B-cell development and regulates B cell identity

Hend Abdelrasoul / Markus Werner / Corinna S. Setz / Klaus Okkenhaug / Hassan Jumaa

Scientific Reports, Vol 8, Iss 1, Pp 1-

2018 Volume 15

Abstract: Abstract Phosphoinositide-3 kinase (PI3K) signaling is important for the survival of numerous cell types and class IA of PI3K is specifically required for the development of B cells but not for T cell development. Here, we show that class IA PI3K- ... ...

Abstract	Abstract Phosphoinositide-3 kinase (PI3K) signaling is important for the survival of numerous cell types and class IA of PI3K is specifically required for the development of B cells but not for T cell development. Here, we show that class IA PI3K-mediated signals induce the expression of the transcription factor Pax5, which plays a central role in B cell commitment and differentiation by activating the expression of central B cell-specific signaling proteins such as SLP-65 and CD19. Defective class IA PI3K function leads to reduction in Pax5 expression and prevents B cell development beyond the stage expressing the precursor B cell receptor (pre-BCR). Investigating the mechanism of PI3K-induced Pax5 expression revealed that it involves a network of transcription factors including FoxO1 and Irf4 that directly binds to the Pax5 gene. Together, our results suggest that PI3K signaling links survival and differentiation of developing B cells with B cell identity and that decreased PI3K activity in pre-B cells results in reduced Pax5 expression and lineage plasticity.
Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2018-01-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: PI3K-Mediated Blimp-1 Activation Controls B Cell Selection and Homeostasis.

Setz, Corinna S / Hug, Eva / Khadour, Ahmad / Abdelrasoul, Hend / Bilal, Mayas / Hobeika, Elias / Jumaa, Hassan

Cell reports

2018 Volume 24, Issue 2, Page(s) 391–405

Abstract: Activation of phosphoinositide 3-kinase (PI3K) signaling plays a central role in regulating proliferation and survival of B cells. Here, we tested the hypothesis that B cell receptor (BCR)-mediated activation of PI3K induces the terminal differentiation ... ...

Abstract	Activation of phosphoinositide 3-kinase (PI3K) signaling plays a central role in regulating proliferation and survival of B cells. Here, we tested the hypothesis that B cell receptor (BCR)-mediated activation of PI3K induces the terminal differentiation factor Blimp-1 that interferes with proliferation and survival, thereby controlling the expansion of activated B cells. In fact, B-cell-specific inactivation of Pten, the negative regulator of PI3K signaling, leads to deregulated PI3K activity and elevated Blimp-1 expression. Combined deficiency for Pten and Blimp-1 results in abnormal expansion of B-1 B cells and splenomegaly. Interestingly, Blimp-1 also acts at early stages of B cell development to regulate B cell selection, as Blimp-1 deficiency results in an increased proportion of autoreactive B cells. Together, our data suggest that the combined requirement of deregulated PI3K signaling in addition to defective terminal differentiation represents the basis for proper selection and expansion of developing B cells.
MeSH term(s)	Animals ; B-Lymphocytes/cytology ; B-Lymphocytes/metabolism ; Cell Compartmentation ; Cell Death ; Cell Differentiation ; Cell Proliferation ; Cytoprotection ; Female ; Homeostasis ; Male ; Mice, Transgenic ; PTEN Phosphohydrolase/deficiency ; PTEN Phosphohydrolase/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Positive Regulatory Domain I-Binding Factor 1/deficiency ; Positive Regulatory Domain I-Binding Factor 1/metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Receptors, Antigen, B-Cell/metabolism
Chemical Substances	Prdm1 protein, mouse ; Proto-Oncogene Proteins c-bcl-2 ; Receptors, Antigen, B-Cell ; Positive Regulatory Domain I-Binding Factor 1 (EC 2.1.1.-) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; PTEN Phosphohydrolase (EC 3.1.3.67)
Language	English
Publishing date	2018-07-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2018.06.035
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Article ; Online: PI3K-Mediated Blimp-1 Activation Controls B Cell Selection and Homeostasis

Corinna S. Setz / Eva Hug / Ahmad Khadour / Hend Abdelrasoul / Mayas Bilal / Elias Hobeika / Hassan Jumaa

Cell Reports, Vol 24, Iss 2, Pp 391-

2018 Volume 405

Abstract: ... B cells. : Setz et al. show that BCR-mediated activation of PI3K induces the terminal differentiation ...

Abstract	Summary: Activation of phosphoinositide 3-kinase (PI3K) signaling plays a central role in regulating proliferation and survival of B cells. Here, we tested the hypothesis that B cell receptor (BCR)-mediated activation of PI3K induces the terminal differentiation factor Blimp-1 that interferes with proliferation and survival, thereby controlling the expansion of activated B cells. In fact, B-cell-specific inactivation of Pten, the negative regulator of PI3K signaling, leads to deregulated PI3K activity and elevated Blimp-1 expression. Combined deficiency for Pten and Blimp-1 results in abnormal expansion of B-1 B cells and splenomegaly. Interestingly, Blimp-1 also acts at early stages of B cell development to regulate B cell selection, as Blimp-1 deficiency results in an increased proportion of autoreactive B cells. Together, our data suggest that the combined requirement of deregulated PI3K signaling in addition to defective terminal differentiation represents the basis for proper selection and expansion of developing B cells. : Setz et al. show that BCR-mediated activation of PI3K induces the terminal differentiation factor Blimp-1 that interferes with cell cycling and survival, thereby preventing the expansion of activated B cells. Thus, the interplay between PI3K activity and regulation of terminal differentiation determines proper selection and expansion of developing B cells. Keywords: autoreactivity, proliferation, B cell development, selection, editing, clonal deletion differentiation, Pten, Blimp-1
Keywords	Biology (General) ; QH301-705.5
Subject code	572
Language	English
Publishing date	2018-07-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Pten controls B-cell responsiveness and germinal center reaction by regulating the expression of IgD BCR.

Setz, Corinna S / Khadour, Ahmad / Renna, Valerio / Iype, Joseena / Gentner, Eva / He, Xiaocui / Datta, Moumita / Young, Marc / Nitschke, Lars / Wienands, Jürgen / Maity, Palash C / Reth, Michael / Jumaa, Hassan

The EMBO journal

2019 Volume 38, Issue 11

Abstract: In contrast to other B-cell antigen receptor (BCR) classes, the function of IgD BCR on mature B cells remains largely elusive as mature B cells co-express IgM, which is sufficient for development, survival, and activation of B cells. Here, we show that ... ...

Abstract	In contrast to other B-cell antigen receptor (BCR) classes, the function of IgD BCR on mature B cells remains largely elusive as mature B cells co-express IgM, which is sufficient for development, survival, and activation of B cells. Here, we show that IgD expression is regulated by the forkhead box transcription factor FoxO1, thereby shifting the responsiveness of mature B cells towards recognition of multivalent antigen. FoxO1 is repressed by phosphoinositide 3-kinase (PI3K) signaling and requires the lipid phosphatase Pten for its activation. Consequently, Pten-deficient B cells expressing knock-ins for BCR
MeSH term(s)	Animals ; B-Lymphocytes/physiology ; Cells, Cultured ; Forkhead Box Protein O1/physiology ; Gene Expression Regulation/immunology ; Germinal Center/metabolism ; Germinal Center/physiology ; Immunoglobulin D/genetics ; Immunoglobulin D/immunology ; Immunoglobulin D/metabolism ; Mice ; Mice, Transgenic ; PTEN Phosphohydrolase/genetics ; PTEN Phosphohydrolase/physiology ; Receptors, Antigen, B-Cell/genetics ; Receptors, Antigen, B-Cell/metabolism ; Signal Transduction/genetics ; Signal Transduction/immunology
Chemical Substances	Forkhead Box Protein O1 ; Foxo1 protein, mouse ; Immunoglobulin D ; Receptors, Antigen, B-Cell ; PTEN Phosphohydrolase (EC 3.1.3.67) ; Pten protein, mouse (EC 3.1.3.67)
Language	English
Publishing date	2019-04-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	586044-1
ISSN	1460-2075 ; 0261-4189
ISSN (online)	1460-2075
ISSN	0261-4189
DOI	10.15252/embj.2018100249
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Zs.A 1808: 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: Human Macrophages Escape Inhibition of Major Histocompatibility Complex-Dependent Antigen Presentation by Cytomegalovirus and Drive Proliferation and Activation of Memory CD4

Frascaroli, Giada / Lecher, Carina / Varani, Stefania / Setz, Corinna / van der Merwe, Johannes / Brune, Wolfram / Mertens, Thomas

Frontiers in immunology

2018 Volume 9, Page(s) 1129

Abstract: Human cytomegalovirus (HCMV) persistently infects 40-90% of the human population but in the face of a normal immune system, viral spread and dissemination are efficiently controlled thus preventing clinically signs and disease. HCMV-infected hosts ... ...

Abstract	Human cytomegalovirus (HCMV) persistently infects 40-90% of the human population but in the face of a normal immune system, viral spread and dissemination are efficiently controlled thus preventing clinically signs and disease. HCMV-infected hosts produce a remarkably large amount of HCMV-specific CD4
MeSH term(s)	Antigen Presentation/immunology ; Antigens, Viral/immunology ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/metabolism ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/metabolism ; Cell Line ; Cytomegalovirus/genetics ; Cytomegalovirus/immunology ; Cytomegalovirus Infections/immunology ; Cytomegalovirus Infections/metabolism ; Cytomegalovirus Infections/virology ; Gene Expression Regulation, Viral ; Humans ; Immunologic Memory ; Lymphocyte Activation/immunology ; Macrophages/immunology ; Macrophages/metabolism ; Macrophages/virology ; Major Histocompatibility Complex/immunology ; Viral Proteins/genetics ; Viral Proteins/immunology
Chemical Substances	Antigens, Viral ; Viral Proteins
Language	English
Publishing date	2018-05-25
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2018.01129
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Article ; Online: Lectins from opportunistic bacteria interact with acquired variable-region glycans of surface immunoglobulin in follicular lymphoma.

Schneider, Dunja / Dühren-von Minden, Marcus / Alkhatib, Alabbas / Setz, Corinna / van Bergen, Cornelis A M / Benkißer-Petersen, Marco / Wilhelm, Isabel / Villringer, Sarah / Krysov, Sergey / Packham, Graham / Zirlik, Katja / Römer, Winfried / Buske, Christian / Stevenson, Freda K / Veelken, Hendrik / Jumaa, Hassan

Blood

2015 Volume 125, Issue 21, Page(s) 3287–3296

Abstract: B-cell antigen receptor (BCR) expression is a key feature of most B-cell lymphomas, but the mechanisms of BCR signal induction and the involvement of autoantigen recognition remain unclear. In follicular lymphoma (FL) B cells, BCR expression is retained ... ...

Abstract	B-cell antigen receptor (BCR) expression is a key feature of most B-cell lymphomas, but the mechanisms of BCR signal induction and the involvement of autoantigen recognition remain unclear. In follicular lymphoma (FL) B cells, BCR expression is retained despite a chromosomal translocation that links the antiapoptotic gene BCL2 to the regulatory elements of immunoglobulin genes, thereby disrupting 1 heavy-chain allele. A remarkable feature of FL-BCRs is the acquisition of potential N-glycosylation sites during somatic hypermutation. The introduced glycans carry mannose termini, which create potential novel binding sites for mannose-specific lectins. Here, we investigated the effect of N-linked variable-region glycosylation for BCR interaction with cognate antigen and with lectins of different origins. N-glycans were found to severely impair BCR specificity and affinity to the initial cognate antigen. In addition, we found that lectins from Pseudomonas aeruginosa and Burkholderia cenocepacia bind and stimulate FL cells. Human exposure to these bacteria can occur by contact with soil and water. In addition, they represent opportunistic pathogens in susceptible hosts. Understanding the role of bacterial lectins might elucidate the pathogenesis of FL and establish novel therapeutic approaches.
MeSH term(s)	Bacterial Infections/complications ; Bacterial Infections/immunology ; Flow Cytometry ; Glycosylation ; Humans ; Immunoglobulin Variable Region/chemistry ; Immunoglobulin Variable Region/immunology ; Lectins/immunology ; Lymphoma, Follicular/complications ; Lymphoma, Follicular/immunology ; Opportunistic Infections/complications ; Opportunistic Infections/immunology ; Polysaccharides/metabolism ; Receptors, Antigen, B-Cell/chemistry ; Receptors, Antigen, B-Cell/immunology ; Receptors, Antigen, B-Cell/metabolism
Chemical Substances	Immunoglobulin Variable Region ; Lectins ; Polysaccharides ; Receptors, Antigen, B-Cell
Language	English
Publishing date	2015-03-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2014-11-609404
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Zs.MO 364: Show issues

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