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Article ; Online: Regulation of the germinal center response by nuclear receptors and implications for autoimmune diseases.

Olson, William J / Jakic, Bojana / Hermann-Kleiter, Natascha

2020 Volume 287, Issue 14, Page(s) 2866–2890

Abstract: The immune system plays an essential role in protecting the host from infectious diseases and cancer. Notably, B and T lymphocytes from the adaptive arm of the immune system can co-operate to form long-lived antibody responses and are therefore the main ... ...

Abstract	The immune system plays an essential role in protecting the host from infectious diseases and cancer. Notably, B and T lymphocytes from the adaptive arm of the immune system can co-operate to form long-lived antibody responses and are therefore the main target in vaccination approaches. Nevertheless, protective immune responses must be tightly regulated to avoid hyper-responsiveness and responses against self that can result in autoimmunity. Nuclear receptors (NRs) are perfectly adapted to rapidly alter transcriptional cellular responses to altered environmental settings. Their functional role is associated with both immune deficiencies and autoimmunity. Despite extensive linking of nuclear receptor function with specific CD4 T helper subsets, research on the functional roles and mechanisms of specific NRs in CD4 follicular T helper cells (Tfh) and germinal center (GC) B cells during the germinal center reaction is just emerging. We review recent advances in our understanding of NR regulation in specific cell types of the GC response and discuss their implications for autoimmune diseases such as systemic lupus erythematosus (SLE).
MeSH term(s)	Animals ; Autoimmune Diseases/immunology ; Autoimmune Diseases/metabolism ; Autoimmune Diseases/pathology ; Autoimmunity/immunology ; Germinal Center/immunology ; Humans ; Lymphocyte Subsets/immunology ; Receptors, Cytoplasmic and Nuclear/immunology ; Receptors, Cytoplasmic and Nuclear/metabolism
Chemical Substances	Receptors, Cytoplasmic and Nuclear
Language	English
Publishing date	2020-04-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.15312
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Article ; Online: Silicone implant surface microtopography modulates inflammation and tissue repair in capsular fibrosis.

Schoberleitner, Ines / Faserl, Klaus / Tripp, Christoph H / Pechriggl, Elisabeth Judith / Sigl, Stephan / Brunner, Andrea / Zelger, Bettina / Hermann-Kleiter, Natascha / Baier, Leoni / Steinkellner, Theresia / Sarg, Bettina / Egle, Daniel / Brunner, Christine / Wolfram, Dolores

Frontiers in immunology

2024 Volume 15, Page(s) 1342895

Abstract: Excessive fibrous capsule formation around silicone mammary implants (SMI) involves immune reactions to silicone. Capsular fibrosis, a common SMI complication linked to host responses, worsens with specific implant topographies. Our study with 10 ... ...

Abstract	Excessive fibrous capsule formation around silicone mammary implants (SMI) involves immune reactions to silicone. Capsular fibrosis, a common SMI complication linked to host responses, worsens with specific implant topographies. Our study with 10 patients investigated intra- and inter-individually, reduced surface roughness effects on disease progression, wound responses, chronic inflammation, and capsular composition. The results illuminate the significant impact of surface roughness on acute inflammatory responses, fibrinogen accumulation, and the subsequent fibrotic cascade. The reduction of surface roughness to an average roughness of 4 μm emerges as a promising approach for mitigating detrimental immune reactions, promoting healthy wound healing, and curbing excessive fibrosis. The identified proteins adhering to rougher surfaces shed light on potential mediators of pro-inflammatory and pro-fibrotic processes, further emphasizing the need for meticulous consideration of surface design. The composition of the implant capsule and the discovery of intracapsular HSP60 expression highlight the intricate web of stress responses and immune activation that can impact long-term tissue outcomes.
MeSH term(s)	Humans ; Prostheses and Implants ; Inflammation ; Silicones ; Fibrosis ; Wound Healing
Chemical Substances	Silicones
Language	English
Publishing date	2024-03-19
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.2024.1342895
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Bacterial Infection with

Jakic, Bojana / Kimpel, Janine / Olson, William J / Labi, Verena / Hermann-Kleiter, Natascha

Bio-protocol

2021 Volume 11, Issue 23, Page(s) e4247

Abstract: Pathogens such as bacteria, viruses, fungi, or protozoa can cause acute and chronic infections in their hosts. The intracellular ... ...

Abstract	Pathogens such as bacteria, viruses, fungi, or protozoa can cause acute and chronic infections in their hosts. The intracellular bacterium
Language	English
Publishing date	2021-12-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	2833269-6
ISSN	2331-8325 ; 2331-8325
ISSN (online)	2331-8325
ISSN	2331-8325
DOI	10.21769/BioProtoc.4247
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Article ; Online: Targeting the orphan nuclear receptor NR2F6 in T cells primes tumors for immune checkpoint therapy.

Klepsch, Victoria / Pommermayr, Maria / Humer, Dominik / Brigo, Natascha / Hermann-Kleiter, Natascha / Baier, Gottfried

Cell communication and signaling : CCS

2020 Volume 18, Issue 1, Page(s) 8

Abstract: Background: NR2F6 has been proposed as an alternative cancer immune checkpoint in the effector T cell compartment. However, a realistic assessment of the in vivo therapeutic potential of NR2F6 requires acute depletion.: Methods: Employing primary T ... ...

Abstract	Background: NR2F6 has been proposed as an alternative cancer immune checkpoint in the effector T cell compartment. However, a realistic assessment of the in vivo therapeutic potential of NR2F6 requires acute depletion. Methods: Employing primary T cells isolated from Cas9-transgenic mice for electroporation of chemically synthesized sgRNA, we established a CRISPR/Cas9-mediated acute knockout protocol of Nr2f6 in primary mouse T cells. Results: Analyzing these Nr2f6 Conclusions: These findings indicate that Nr2f6
MeSH term(s)	Animals ; Base Sequence ; CRISPR-Cas Systems/genetics ; CTLA-4 Antigen/metabolism ; Cells, Cultured ; Gene Deletion ; Immune Checkpoint Inhibitors/pharmacology ; Immune Checkpoint Inhibitors/therapeutic use ; Immunity/drug effects ; Mice, Inbred C57BL ; Mutagenesis/genetics ; Neoplasms/drug therapy ; Neoplasms/immunology ; Neoplasms/pathology ; Programmed Cell Death 1 Receptor/metabolism ; RNA, Guide, CRISPR-Cas Systems/metabolism ; Repressor Proteins/deficiency ; Repressor Proteins/metabolism ; Reproducibility of Results ; T-Lymphocytes/drug effects ; T-Lymphocytes/immunology
Chemical Substances	CTLA-4 Antigen ; Immune Checkpoint Inhibitors ; Nr2f6 protein, mouse ; Programmed Cell Death 1 Receptor ; RNA, Guide, CRISPR-Cas Systems ; Repressor Proteins
Language	English
Publishing date	2020-01-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2126315-2
ISSN	1478-811X ; 1478-811X
ISSN (online)	1478-811X
ISSN	1478-811X
DOI	10.1186/s12964-019-0454-z
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Article ; Online: A role for the nuclear receptor NR2F6 in peritoneal B cell homeostasis.

Olson, William J / Jakic, Bojana / Labi, Verena / Woelk, Johannes / Derudder, Emmanuel / Baier, Gottfried / Hermann-Kleiter, Natascha

Frontiers in immunology

2022 Volume 13, Page(s) 845235

Abstract: B cells are key mediators of humoral immunity. Mature B cells fall into various sub-classes that can be separated by their ontogeny, expression of cell surface markers, anatomical location, and function. B1 subsets play important roles in natural ... ...

Abstract	B cells are key mediators of humoral immunity. Mature B cells fall into various sub-classes that can be separated by their ontogeny, expression of cell surface markers, anatomical location, and function. B1 subsets play important roles in natural immunity and constitute the majority of B cells in newborns. In the adult, B1 cells predominate in the pleural and peritoneal cavities, while the mature B2 follicular subset makes up the major fraction of B cells in lymphoid tissue, although important subsets of antibody-secreting B1 cells are also present at these sites. B1 cells are the main producers of natural IgM but can also contribute to elimination of some pathogens, while B2 cells primarily mediate response to foreign antigens. The differential molecular underpinning of the B1 and B2 subsets remains incompletely understood. Here we demonstrate that germline-deficiency of the orphan nuclear receptor NR2F6 causes a partial loss of B1b and B2 B cells in the peritoneum while leaving peritoneal B1a cells unaltered. A competitive bone marrow chimera in
MeSH term(s)	Animals ; B-Lymphocytes ; Homeostasis ; Mice ; Peritoneal Cavity ; Peritoneum ; Receptors, Cytoplasmic and Nuclear ; Repressor Proteins/metabolism
Chemical Substances	Nr2f6 protein, mouse ; Receptors, Cytoplasmic and Nuclear ; Repressor Proteins
Language	English
Publishing date	2022-08-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.845235
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Article ; Online: Loss of the orphan nuclear receptor NR2F6 enhances CD8

Jakic, Bojana / Olson, William J / Siegmund, Kerstin / Klepsch, Victoria / Kimpel, Janine / Labi, Verena / Zehn, Dietmar / Baier, Gottfried / Hermann-Kleiter, Natascha

Cell death & disease

2021 Volume 12, Issue 2, Page(s) 187

Abstract: Memory formation is a hallmark of T cell-mediated immunity, but how differentiation into either short-lived effector cells (SLECs, ... ...

Abstract	Memory formation is a hallmark of T cell-mediated immunity, but how differentiation into either short-lived effector cells (SLECs, CD127
Language	English
Publishing date	2021-02-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-021-03470-9
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Article: Regulation of the germinal center response by nuclear receptors and implications for autoimmune diseases

Olson, William J / Jakic, Bojana / Hermann‐Kleiter, Natascha

FEBS journal. 2020 July, v. 287, no. 14

2020

Abstract: The immune system plays an essential role in protecting the host from infectious diseases and cancer. Notably, B and T lymphocytes from the adaptive arm of the immune system can co‐operate to form long‐lived antibody responses and are therefore the main ... ...

Abstract	The immune system plays an essential role in protecting the host from infectious diseases and cancer. Notably, B and T lymphocytes from the adaptive arm of the immune system can co‐operate to form long‐lived antibody responses and are therefore the main target in vaccination approaches. Nevertheless, protective immune responses must be tightly regulated to avoid hyper‐responsiveness and responses against self that can result in autoimmunity. Nuclear receptors (NRs) are perfectly adapted to rapidly alter transcriptional cellular responses to altered environmental settings. Their functional role is associated with both immune deficiencies and autoimmunity. Despite extensive linking of nuclear receptor function with specific CD4 T helper subsets, research on the functional roles and mechanisms of specific NRs in CD4 follicular T helper cells (Tfh) and germinal center (GC) B cells during the germinal center reaction is just emerging. We review recent advances in our understanding of NR regulation in specific cell types of the GC response and discuss their implications for autoimmune diseases such as systemic lupus erythematosus (SLE).
Keywords	CD4-positive T-lymphocytes ; antibodies ; autoimmunity ; lupus erythematosus ; lymph nodes ; transcription (genetics) ; vaccination
Language	English
Dates of publication	2020-07
Size	p. 2866-2890.
Publishing place	John Wiley & Sons, Ltd
Document type	Article
Note	NAL-AP-2-clean ; REVIEW
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.15312
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Targeting the orphan nuclear receptor NR2F6 in T cells primes tumors for immune checkpoint therapy

Victoria Klepsch / Maria Pommermayr / Dominik Humer / Natascha Brigo / Natascha Hermann-Kleiter / Gottfried Baier

Cell Communication and Signaling, Vol 18, Iss 1, Pp 1-

2020 Volume 12

Abstract: Abstract Background NR2F6 has been proposed as an alternative cancer immune checkpoint in the effector T cell compartment. However, a realistic assessment of the in vivo therapeutic potential of NR2F6 requires acute depletion. Methods Employing primary T ...

Abstract	Abstract Background NR2F6 has been proposed as an alternative cancer immune checkpoint in the effector T cell compartment. However, a realistic assessment of the in vivo therapeutic potential of NR2F6 requires acute depletion. Methods Employing primary T cells isolated from Cas9-transgenic mice for electroporation of chemically synthesized sgRNA, we established a CRISPR/Cas9-mediated acute knockout protocol of Nr2f6 in primary mouse T cells. Results Analyzing these Nr2f6 CRISPR/Cas9 knockout T cells, we reproducibly observed a hyper-reactive effector phenotype upon CD3/CD28 stimulation in vitro, highly reminiscent to Nr2f6 −/− T cells. Importantly, CRISPR/Cas9-mediated Nr2f6 ablation prior to adoptive cell therapy (ACT) of autologous polyclonal T cells into wild-type tumor-bearing recipient mice in combination with PD-L1 or CTLA-4 tumor immune checkpoint blockade significantly delayed MC38 tumor progression and induced superior survival, thus further validating a T cell-inhibitory function of NR2F6 during tumor progression. Conclusions These findings indicate that Nr2f6 CRISPR/Cas9 knockout T cells are comparable to germline Nr2f6 −/− T cells, a result providing an independent confirmation of the immune checkpoint function of lymphatic NR2F6. Taken together, CRISPR/Cas9-mediated acute Nr2f6 gene ablation in primary mouse T cells prior to ACT appeared feasible for potentiating established PD-L1 and CTLA-4 blockade therapies, thereby pioneering NR2F6 inhibition as a sensitizing target for augmented tumor regression. Video abstract. Graphical abstract
Keywords	Immune checkpoint NR2F6 ; transcriptional repressor of CD3+ effector T cell functions ; CRISPR/Cas9 genetically modified cell therapy ; Combinatorial treatment regimens ; Medicine ; R ; Cytology ; QH573-671
Language	English
Publishing date	2020-01-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Orphan nuclear receptor NR2F6 acts as an essential gatekeeper of Th17 CD4+ T cell effector functions.

Hermann-Kleiter, Natascha / Baier, Gottfried

Cell communication and signaling : CCS

2014 Volume 12, Page(s) 38

Abstract: Members of the evolutionarily conserved family of the chicken ovalbumin upstream promoter transcription factor NR2F/COUP-TF orphan receptors have been implicated in lymphocyte biology, ranging from activation to differentiation and elicitation of immune ... ...

Abstract	Members of the evolutionarily conserved family of the chicken ovalbumin upstream promoter transcription factor NR2F/COUP-TF orphan receptors have been implicated in lymphocyte biology, ranging from activation to differentiation and elicitation of immune effector functions. In particular, a CD4+ T cell intrinsic and non-redundant function of NR2F6 as a potent and selective repressor of the transcription of the pro-inflammatory cytokines interleukin (Il) 2, interferon y (ifng) and consequently of T helper (Th)17 CD4+ T cell-mediated autoimmune disorders has been discovered. NR2F6 serves as an antigen receptor signaling threshold-regulated barrier against autoimmunity where NR2F6 is part of a negative feedback loop that limits inflammatory tissue damage induced by weakly immunogenic antigens such as self-antigens. Under such low affinity antigen receptor stimulation, NR2F6 appears as a prototypical repressor that functions to "lock out" harmful Th17 lineage effector transcription. Mechanistically, only sustained high affinity antigen receptor-induced protein kinase C (PKC)-mediated phosphorylation has been shown to inactivate NR2F6, thereby displacing pre-bound NR2F6 from the DNA and, subsequently, allowing for robust NFAT/AP-1- and RORγt-mediated cytokine transcription. The NR2F6 target gene repertoire thus identifies a general anti-inflammatory gatekeeper role for this orphan receptor. Investigating these signaling pathway(s) will enable a greater knowledge of the genetic, immune, and environmental mechanisms that lead to chronic inflammation and of certain autoimmune disorders in a given individual.
MeSH term(s)	Animals ; Autoimmunity ; COUP Transcription Factors/chemistry ; COUP Transcription Factors/genetics ; COUP Transcription Factors/metabolism ; Cytokines/genetics ; Cytokines/metabolism ; Humans ; Inflammation/immunology ; Inflammation/metabolism ; Th17 Cells/immunology ; Th17 Cells/metabolism ; Transcription, Genetic
Chemical Substances	COUP Transcription Factors ; Cytokines
Language	English
Publishing date	2014-06-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2126315-2
ISSN	1478-811X ; 1478-811X
ISSN (online)	1478-811X
ISSN	1478-811X
DOI	10.1186/1478-811X-12-38
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Article ; Online: Tumor-targeted therapy with BRAF-inhibitor recruits activated dendritic cells to promote tumor immunity in melanoma.

Journal for immunotherapy of cancer

2024 Volume 12, Issue 4

Abstract: Background: Tumor-targeted therapy causes impressive tumor regression, but the emergence of resistance limits long-term survival benefits in patients. Little information is available on the role of the myeloid cell network, especially dendritic cells ( ... ...

Abstract	Background: Tumor-targeted therapy causes impressive tumor regression, but the emergence of resistance limits long-term survival benefits in patients. Little information is available on the role of the myeloid cell network, especially dendritic cells (DC) during tumor-targeted therapy. Methods: Here, we investigated therapy-mediated immunological alterations in the tumor microenvironment (TME) and tumor-draining lymph nodes (LN) in the D4M.3A preclinical melanoma mouse model (harboring the V-Raf murine sarcoma viral oncogene homolog B (BRAF) Results: Our findings reveal that BRAF-inhibitor therapy increased tumor immunogenicity, reflected by an upregulation of genes associated with immune activation. The T cell-inflamed TME contained higher numbers of activated cDC1 and cDC2 but also inflammatory CCR2-expressing monocytes. At the same time, tumor-targeted therapy enhanced the frequency of migratory, activated DC subsets in tumor-draining LN. Even more, we identified a cDC2 population expressing the Fc gamma receptor I (FcγRI)/CD64 in tumors and LN that displayed high levels of CD40 and CCR7 indicating involvement in T cell-mediated tumor immunity. The importance of cDC2 is underlined by just a partial loss of therapy response in a cDC1-deficient mouse model. Both CD4 Conclusion: Our results give novel insights into the remodeling of the myeloid landscape by tumor-targeted therapy. We demonstrate that the transient immunogenic tumor milieu contains more activated DC. This knowledge has important implications for the development of future combinatorial therapies.
Language	English
Publishing date	2024-04-17
Publishing country	England
Document type	Journal Article
ZDB-ID	2719863-7
ISSN	2051-1426 ; 2051-1426
ISSN (online)	2051-1426
ISSN	2051-1426
DOI	10.1136/jitc-2023-008606
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