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Article ; Online: Editorial to special issue: monocytes in homeostasis and disease.

Getts, Daniel R

2014 Volume 291, Issue 1-2, Page(s) 1–2

MeSH term(s)	Animals ; Homeostasis ; Humans ; Mice ; Monocytes/cytology ; Monocytes/physiology
Language	English
Publishing date	2014-09
Publishing country	Netherlands
Document type	Editorial
ZDB-ID	80094-6
ISSN	1090-2163 ; 0008-8749
ISSN (online)	1090-2163
ISSN	0008-8749
DOI	10.1016/j.cellimm.2014.10.001
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Zs.A 417: Show issues

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Article: Immune Modifying Effect of Drug Free Biodegradable Nanoparticles on Disease Course of Experimental Autoimmune Neuritis.

Elahi, Ehsan / Ali, Mohamed Ehab / Zimmermann, Julian / Getts, Daniel R / Müller, Marcus / Lamprecht, Alf

Pharmaceutics

2022 Volume 14, Issue 11

Abstract: Guillain-Barre syndrome (GBS) is an autoimmune disease of demyelination and inflammation of peripheral nerves. Current treatments are limited to plasma exchange and intravenous immunoglobulins. Cargo-free nanoparticles (NPs) have been evaluated here for ... ...

Abstract	Guillain-Barre syndrome (GBS) is an autoimmune disease of demyelination and inflammation of peripheral nerves. Current treatments are limited to plasma exchange and intravenous immunoglobulins. Cargo-free nanoparticles (NPs) have been evaluated here for their therapeutic benefit on the disease course of experimental autoimmune neuritis (EAN), mimicking the human GBS. NPs prepared from poly-lactic co-glycolic acid (PLGA) with variable size and surface charge (i.e., 500 nm vs. 130 nm, polyvinyl alcohol (PVA) vs. sodium cholate), were intravenously administered in before- or early-onset treatment schedules in a rat EAN model. NP treatment mitigated distinctly the clinical severity of EAN as compared to the P2-peptide control group (P2) in all treatments and reduced the trafficking of inflammatory monocytes at inflammatory loci and diverted them towards the spleen. Therapeutic treatment with NPs reduced the expression of proinflammatory markers (CD68 (P2: 34.8 ± 6.6 vs. NP: 11.9 ± 2.3), IL-1β (P2: 18.3 ± 0.8 vs. NP: 5.8 ± 2.2), TNF-α (P2: 23.5 ± 3.7 vs. NP: 8.3 ± 1.7) and elevated the expression levels of anti-inflammatory markers CD163 (P2: 19.7 ± 3.0 vs. NP: 41.1 ± 6.5; all for NP-PVA of 130 nm; relative to healthy control). These results highlight the therapeutic potential of such cargo-free NPs in treating EAN, which would be easily translatable into clinical use due to their well-known low-toxicity profile.
Language	English
Publishing date	2022-11-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527217-2
ISSN	1999-4923
ISSN	1999-4923
DOI	10.3390/pharmaceutics14112410
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Article ; Online: Central role of B cells in interleukin-23 dependent neuroinflammation in the GF-IL23 model.

Nitsch, Louisa / Petzinna, Simon / Zimmermann, Julian / Getts, Daniel R / Becker, Albert / Müller, Marcus

Neuroreport

2022 Volume 33, Issue 13, Page(s) 577–582

Abstract: Interleukin (IL)-23 is one of the critical cytokines in autoimmune neuroinflammation. To further clarify the local function of IL-23 on the course of neuroinflammation, we recently established a transgenic mouse model with astrocyte-specific expression ... ...

Abstract	Interleukin (IL)-23 is one of the critical cytokines in autoimmune neuroinflammation. To further clarify the local function of IL-23 on the course of neuroinflammation, we recently established a transgenic mouse model with astrocyte-specific expression of IL-23 (GF-IL23). The GF-IL23 mice spontaneously developed a progressive ataxic phenotype with cerebellar infiltration with high amounts of B cells most prominent in the subarachnoid and perivascular space. To enlighten the B cell role in GF-IL23 mice, we generated GF-IL23 mice on a B cell knockout (k.o.) background (GF-IL23 B cell k.o.). GF-IL23 B cell k.o. mice compared with GF-IL23 mice had no infiltrates or only minor infiltration, and no antibody deposition was detected in the cerebellum. Furthermore, microglia, astrocyte activation, hypervascularization and demyelination were reduced in GF-IL23 B cell k.o. mice compared with GF-IL23 mice. Cytokines and chemokine receptors like IL-12a, cerebrospinal fluid 2 and CXCR3 were downregulated. Our study indicates that B cells are essential in IL-23-dependent neuroinflammation in the GF-IL23 model.
MeSH term(s)	Animals ; B-Lymphocytes/metabolism ; Cytokines/metabolism ; Interleukin-23/genetics ; Interleukin-23/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neuroinflammatory Diseases
Chemical Substances	Cytokines ; Interleukin-23
Language	English
Publishing date	2022-07-18
Publishing country	England
Document type	Journal Article
ZDB-ID	1049746-8
ISSN	1473-558X ; 0959-4965
ISSN (online)	1473-558X
ISSN	0959-4965
DOI	10.1097/WNR.0000000000001818
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Zs.A 3118: Show issues

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Article ; Online: MOG-Specific T Cells Lead to Spontaneous EAE with Multilocular B Cell Infiltration in the GF-IL23 Model.

Nitsch, Louisa / Petzinna, Simon / Zimmermann, Julian / Getts, Daniel R / Becker, Albert / Müller, Marcus

Neuromolecular medicine

2022 Volume 24, Issue 4, Page(s) 415–423

Abstract: Although IL-23 and downstream signal transduction play essential roles in neuroinflammation, the local impact of IL-23 in multiple sclerosis is still not fully understood. Our previous study revealed that the central nervous system (CNS)-restricted ... ...

Abstract	Although IL-23 and downstream signal transduction play essential roles in neuroinflammation, the local impact of IL-23 in multiple sclerosis is still not fully understood. Our previous study revealed that the central nervous system (CNS)-restricted expression of IL-23 in a mouse model with astrocyte-specific expression of IL-23, called GF-IL23 mice, leads to spontaneous formation of infiltrates in the brain, especially in the cerebellum. To further investigate the impact of CNS-specific IL-23-expression on neuroinflammation, we studied the GF-IL23 model in mice expressing a myelin oligodendrocyte glycoprotein (MOG)-specific T cell receptor (GF23-2D2 mice). The GF23-2D2 mice developed a chronic progressive experimental autoimmune encephalomyelitis with myelitis and ataxia without requiring additional immunization. CNS-production of IL-23 alone induced pronounced neuroinflammation in the transgenic MOG-specific T cell receptor model. The GF23-2D2 mice spontaneously developed multilocular infiltrates with a high number of B cells, demyelination and a proinflammatory cytokine milieu indicating that the interaction of encephalitogenic T cells and B cells via co-stimulatory factors seemed to be crucial.
MeSH term(s)	Animals ; Mice ; Encephalomyelitis, Autoimmune, Experimental ; Myelin-Oligodendrocyte Glycoprotein ; T-Lymphocytes ; Receptors, Antigen, T-Cell ; Interleukin-23 ; Mice, Inbred C57BL
Chemical Substances	Myelin-Oligodendrocyte Glycoprotein ; Receptors, Antigen, T-Cell ; Interleukin-23
Language	English
Publishing date	2022-03-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2077809-0
ISSN	1559-1174 ; 1535-1084
ISSN (online)	1559-1174
ISSN	1535-1084
DOI	10.1007/s12017-022-08705-2
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Zs.A 5818: Show issues

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Article ; Online: Implications of T cell receptor biology on the development of new T cell therapies for cancer.

Hardy, Ian R / Schamel, Wolfgang W / Baeuerle, Patrick A / Getts, Daniel R / Hofmeister, Robert

Immunotherapy

2020 Volume 12, Issue 1, Page(s) 89–103

Abstract: Recently, two chimeric antigen receptor (CAR) T cell therapies were approved based on their remarkable efficacy in patients with hematological malignancies. By contrast, CAR-T cell therapies results in solid tumors have been less promising. To develop ... ...

Abstract	Recently, two chimeric antigen receptor (CAR) T cell therapies were approved based on their remarkable efficacy in patients with hematological malignancies. By contrast, CAR-T cell therapies results in solid tumors have been less promising. To develop the next generation of T cell therapies a better understanding of T cell receptor (TCR) biology and its implication for the design of synthetic receptors is critical. Here, we review current and newly developed forms of T cell therapies and how their utilization of different components of the TCR signaling machinery and their requirement for engagement (or not) of human leukocyte antigen impacts their design, efficacy and applicability as cancer drugs. Notably, we highlight the development of human leukocyte antigen-independent T cell platforms that utilize the full TCR complex as having promise to overcome some of the limitations of existing T cell therapies.
MeSH term(s)	Animals ; Cancer Vaccines/immunology ; Humans ; Immunotherapy, Adoptive/methods ; Molecular Targeted Therapy ; Neoplasms/immunology ; Neoplasms/therapy ; Protein Engineering ; Receptors, Antigen, T-Cell/genetics ; Receptors, Antigen, T-Cell/metabolism ; Signal Transduction ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism
Chemical Substances	Cancer Vaccines ; Receptors, Antigen, T-Cell
Language	English
Publishing date	2020-01-06
Publishing country	England
Document type	Journal Article ; Review
ISSN	1750-7448
ISSN (online)	1750-7448
DOI	10.2217/imt-2019-0046
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Article ; Online: Synthetic T cell receptor-based lymphocytes for cancer therapy.

Getts, Daniel / Hofmeister, Robert / Quintás-Cardama, Alfonso

Advanced drug delivery reviews

2019 Volume 141, Page(s) 47–54

Abstract: Chimeric antigen receptor (CAR) T cells have been remarkably successful in patients with hematological malignancies expressing the CD19 surface antigen, but such level of success is far from being replicated in solid tumors. Engineered T cell receptor ( ... ...

Abstract	Chimeric antigen receptor (CAR) T cells have been remarkably successful in patients with hematological malignancies expressing the CD19 surface antigen, but such level of success is far from being replicated in solid tumors. Engineered T cell receptor (TCR) T cells targeting cancer antigens were first developed over two decades ago and represent an alternative adoptive T cell approach that has produced provocative clinical data in solid cancers. However, several factors may hinder this technology from realizing its full potential, including the need for HLA matching, HLA downregulation by cancer cells, the suppressive tumor microenvironment, and tissue liabilities resulting from targeting antigens shared with normal tissues. Efforts therefore continue to engineer enhanced versions of CAR T and TCR T therapies that can overcome current barriers. Furthermore, emergent novel TCR-based, HLA-unrestricted platforms may also provide unique tools that integrate the complexity of the TCR signaling cascade that can be applied to treat solid tumors. This article reviews the current state of development of TCR T cell approaches and discusses next generation improvements to overcome their current limitations.
MeSH term(s)	Animals ; Antigens/immunology ; Humans ; Immunotherapy, Adoptive ; Neoplasms/immunology ; Neoplasms/therapy ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/immunology
Chemical Substances	Antigens ; Receptors, Antigen, T-Cell
Language	English
Publishing date	2019-04-12
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	639113-8
ISSN	1872-8294 ; 0169-409X
ISSN (online)	1872-8294
ISSN	0169-409X
DOI	10.1016/j.addr.2019.04.002
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Zs.A 2241: Show issues

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Article ; Online: Astrocyte-specific expression of interleukin 23 leads to an aggravated phenotype and enhanced inflammatory response with B cell accumulation in the EAE model.

Nitsch, Louisa / Petzinna, Simon / Zimmermann, Julian / Schneider, Linda / Krauthausen, Marius / Heneka, Michael T / Getts, Daniel R / Becker, Albert / Müller, Marcus

Journal of neuroinflammation

2021 Volume 18, Issue 1, Page(s) 101

Abstract: Background: Interleukin 23 is a critical cytokine in the pathogenesis of multiple sclerosis. But the local impact of interleukin 23 on the course of neuroinflammation is still not well defined. To further characterize the effect of interleukin 23 on CNS ...

Abstract	Background: Interleukin 23 is a critical cytokine in the pathogenesis of multiple sclerosis. But the local impact of interleukin 23 on the course of neuroinflammation is still not well defined. To further characterize the effect of interleukin 23 on CNS inflammation, we recently described a transgenic mouse model with astrocyte-specific expression of interleukin 23 (GF-IL23 mice). The GF-IL23 mice spontaneously develop a progressive ataxic phenotype with cerebellar tissue destruction and inflammatory infiltrates with high amounts of B cells most prominent in the subarachnoid and perivascular space. Methods: To further elucidate the local impact of the CNS-specific interleukin 23 synthesis in autoimmune neuroinflammation, we induced a MOG35-55 experimental autoimmune encephalomyelitis (EAE) in GF-IL23 mice and WT mice and analyzed the mice by histology, flow cytometry, and transcriptome analysis. Results: We were able to demonstrate that local interleukin 23 production in the CNS leads to aggravation and chronification of the EAE course with a severe paraparesis and an ataxic phenotype. Moreover, enhanced multilocular neuroinflammation was present not only in the spinal cord, but also in the forebrain, brainstem, and predominantly in the cerebellum accompanied by persisting demyelination. Thereby, interleukin 23 creates a pronounced proinflammatory response with accumulation of leukocytes, in particular B cells, CD4+ cells, but also γδ T cells and activated microglia/macrophages. Furthermore, transcriptome analysis revealed an enhanced proinflammatory cytokine milieu with upregulation of lymphocyte activation markers, co-stimulatory markers, chemokines, and components of the complement system. Conclusion: Taken together, the GF-IL23 model allowed a further breakdown of the different mechanisms how IL-23 drives neuroinflammation in the EAE model and proved to be a useful tool to further dissect the impact of interleukin 23 on neuroinflammatory models.
MeSH term(s)	Animals ; Astrocytes/immunology ; Astrocytes/metabolism ; B-Lymphocytes/immunology ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Encephalomyelitis, Autoimmune, Experimental/metabolism ; Encephalomyelitis, Autoimmune, Experimental/pathology ; Inflammation/immunology ; Inflammation/metabolism ; Interleukin-23/immunology ; Interleukin-23/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Phenotype
Chemical Substances	Interleukin-23
Language	English
Publishing date	2021-04-27
Publishing country	England
Document type	Journal Article
ISSN	1742-2094
ISSN (online)	1742-2094
DOI	10.1186/s12974-021-02140-z
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Article ; Online: Chapter 21 Microbial Infection as a Trigger of T-Cell Autoimmunity

Getts, Daniel R. / Spiteri, Alanna / King, Nicholas J.C. / Miller, Stephen D.

2020

Abstract: Autoimmunity is a significant health concern with diseases such as type 1 diabetes, rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis, drastically increasing in prevalence over the last 30–40 years. The precise trigger for ... ...

Abstract	Autoimmunity is a significant health concern with diseases such as type 1 diabetes, rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis, drastically increasing in prevalence over the last 30–40 years. The precise trigger for autoimmunity is unknown, although genetics clearly plays a significant role. However, low concordance rates in monozygotic twins as well as geographical distribution patterns suggest that the development of autoimmunity is the culmination of multiple factors, with genetic predisposition being only one component. Retrospective epidemiological and animal studies have shown that infection is an important factor in the generation of autoimmune disease. Traditionally, cross-reactive T-cell recognition, known as molecular mimicry, as well as bystander T-cell activation culminating in epitope spreading are considered the predominant mechanisms through which infection may culminate in an autoimmune response. Notwithstanding, recent studies suggest other avenues, including microbial toxins and virus-induced decoy of the immune system, may also play a role. In this chapter, the relationship between antimicrobial immune responses and development of autoimmune disease will be reviewed.
Keywords	COVID-19 ; Coronavirus ; covid19
Language	English
Publishing date	2020-01-01
Publishing country	au
Document type	Article ; Online
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Article ; Online: TAK-101 Nanoparticles Induce Gluten-Specific Tolerance in Celiac Disease: A Randomized, Double-Blind, Placebo-Controlled Study.

Kelly, Ciarán P / Murray, Joseph A / Leffler, Daniel A / Getts, Daniel R / Bledsoe, Adam C / Smithson, Glennda / First, M Roy / Morris, Amy / Boyne, Michael / Elhofy, Adam / Wu, Tsung-Teh / Podojil, Joseph R / Miller, Stephen D

Gastroenterology

2021 Volume 161, Issue 1, Page(s) 66–80.e8

Abstract: Background & aims: In celiac disease (CeD), gluten induces immune activation, leading to enteropathy. TAK-101, gluten protein (gliadin) encapsulated in negatively charged poly(dl-lactide-co-glycolic acid) nanoparticles, is designed to induce gluten- ... ...

Abstract	Background & aims: In celiac disease (CeD), gluten induces immune activation, leading to enteropathy. TAK-101, gluten protein (gliadin) encapsulated in negatively charged poly(dl-lactide-co-glycolic acid) nanoparticles, is designed to induce gluten-specific tolerance. Methods: TAK-101 was evaluated in phase 1 dose escalation safety and phase 2a double-blind, randomized, placebo-controlled studies. Primary endpoints included pharmacokinetics, safety, and tolerability of TAK-101 (phase 1) and change from baseline in circulating gliadin-specific interferon-γ-producing cells at day 6 of gluten challenge, in patients with CeD (phase 2a). Secondary endpoints in the phase 2a study included changes from baseline in enteropathy (villus height to crypt depth ratio [Vh:Cd]), and frequency of intestinal intraepithelial lymphocytes and peripheral gut-homing T cells. Results: In phase 2a, 33 randomized patients completed the 14-day gluten challenge. TAK-101 induced an 88% reduction in change from baseline in interferon-γ spot-forming units vs placebo (2.01 vs 17.58, P = .006). Vh:Cd deteriorated in the placebo group (-0.63, P = .002), but not in the TAK-101 group (-0.18, P = .110), although the intergroup change from baseline was not significant (P = .08). Intraepithelial lymphocyte numbers remained equal. TAK-101 reduced changes in circulating α4β7 Conclusions: TAK-101 was well tolerated and prevented gluten-induced immune activation in CeD. The findings from the present clinical trial suggest that antigen-specific tolerance was induced and represent a novel approach translatable to other immune-mediated diseases. ClinicalTrials.gov identifiers: NCT03486990 and NCT03738475.
MeSH term(s)	Celiac Disease/immunology ; Celiac Disease/pathology ; Double-Blind Method ; Gliadin/administration & dosage ; Gliadin/immunology ; Glycolates/administration & dosage ; Humans ; Immune Tolerance/immunology ; Infusions, Intravenous ; Nanoparticles/administration & dosage
Chemical Substances	Glycolates ; Poly D,L-Lactide-Co-Glycolic Acid ; Gliadin (9007-90-3)
Language	English
Publishing date	2021-03-17
Publishing country	United States
Document type	Clinical Trial, Phase I ; Clinical Trial, Phase II ; Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
ZDB-ID	80112-4
ISSN	1528-0012 ; 0016-5085
ISSN (online)	1528-0012
ISSN	0016-5085
DOI	10.1053/j.gastro.2021.03.014
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Article ; Online: Deficient Natural Killer Dendritic Cell Responses Underlay the Induction of Theiler's Virus-Induced Autoimmunity.

Chastain, Emily M L / Getts, Daniel R / Miller, Stephen D

mBio

2015 Volume 6, Issue 4, Page(s) e01175

Abstract: Unlabelled: The initiating events in autoimmune disease remain to be completely understood, but it is thought that genetic predisposition synergizes with "environmental" factors, including viral infection, leading to disease. One elegant animal model ... ...

Abstract	Unlabelled: The initiating events in autoimmune disease remain to be completely understood, but it is thought that genetic predisposition synergizes with "environmental" factors, including viral infection, leading to disease. One elegant animal model used to study the pathogenesis of multiple sclerosis that perfectly blends genetics and environmental components in the context of virus-induced autoimmunity is Theiler's murine encephalitis virus-induced demyelinating disease (TMEV-IDD). TMEV-infected disease-susceptible SJL/J mice develop a persistent central nervous system (CNS) infection and later develop autoimmune demyelination, while disease-resistant C57BL/6 (B6) mice rapidly clear the infection and develop no autoimmune pathology. Mice of the (B6 × SJL/J)F1 cross between these two mouse strains are classified as intermediately susceptible. We employed this model to investigate if rapid virus clearance in B6 versus SJL/J mice was perhaps related to differences in the innate immune response in the CNS of the two strains in the first few days following intracerebral virus inoculation. Here we show that SJL/J mice lack, in addition to NK cells, a novel innate immune subset known as natural killer dendritic cells (NKDCs), which express phenotypic markers (CD11c(int) NK1.1(+)) and functional activity of both NK cells and DCs. These NKDCs are activated in the periphery and migrate into the infected CNS in a very late antigen 4 (VLA-4)-dependent fashion. Most significantly, NKDCs are critical for CNS clearance of TMEV, as transfer of NKDCs purified from B6 mice into TMEV-IDD-susceptible (B6 × SJL/J)F1 mice promotes viral clearance. Together the findings of this work show for the first time a link between NKDCs, viral infection, and CNS autoimmunity. Importance: Viral infection is an important cofactor, along with genetic susceptibility, in the initiation of a variety of organ-specific autoimmune diseases. Thus, in-depth understanding of how virus infections trigger autoimmunity may lead to novel ways to prevent or treat these diseases. Theiler's murine encephalitis virus-induced demyelinating disease (TMEV-IDD) serves as an important model for the human T cell-mediated autoimmune demyelinating disease multiple sclerosis. Induction of TMEV-IDD is genetically controlled as SJL/J mice develop persistent central nervous system (CNS) infection leading to chronic autoimmune demyelination, while C57BL/6 mice rapidly clear virus and are disease resistant. We determined that, as opposed to resistant B6 mice, disease-susceptible SJL/J mice lacked a unique innate immune population, the natural killer dendritic cell (NKDC), which was shown to play a critical role in early CNS virus clearance via its ability to both present virus antigen to T cells and to lyse target cells.
MeSH term(s)	Animals ; Antigens, Ly/analysis ; Autoimmunity ; CD11 Antigens/analysis ; Crosses, Genetic ; Dendritic Cells/chemistry ; Dendritic Cells/immunology ; Dendritic Cells/virology ; Disease Models, Animal ; Immunophenotyping ; Mice ; NK Cell Lectin-Like Receptor Subfamily B/analysis ; Poliomyelitis/immunology ; Poliomyelitis/pathology ; Theilovirus/immunology
Chemical Substances	Antigens, Ly ; CD11 Antigens ; Klrb1c protein, mouse ; NK Cell Lectin-Like Receptor Subfamily B
Language	English
Publishing date	2015-08-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mBio.01175-15
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