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Article ; Online: Synthetic Cell-Based Immunotherapies for Neurologic Diseases.

von Baumgarten, Louisa / Stauss, Hans J / Lünemann, Jan D

Neurology(R) neuroimmunology & neuroinflammation

2023 Volume 10, Issue 5

Abstract: The therapeutic success and widespread approval of genetically engineered T cells for a variety of hematologic malignancies spurred the development of synthetic cell-based immunotherapies for CNS lymphoma, primary brain tumors, and a growing spectrum of ... ...

Abstract	The therapeutic success and widespread approval of genetically engineered T cells for a variety of hematologic malignancies spurred the development of synthetic cell-based immunotherapies for CNS lymphoma, primary brain tumors, and a growing spectrum of nononcologic disease conditions of the nervous system. Chimeric antigen receptor effector T cells bear the potential to deplete target cells with higher efficacy, better tissue penetration, and greater depth than antibody-based cell depletion therapies. In multiple sclerosis and other autoimmune disorders, engineered T-cell therapies are being designed and currently tested in clinical trials for their safety and efficacy to eliminate pathogenic B-lineage cells. Chimeric autoantibody receptor T cells expressing a disease-relevant autoantigen as cell surface domains are designed to selectively deplete autoreactive B cells. Alternative to cell depletion, synthetic antigen-specific regulatory T cells can be engineered to locally restrain inflammation, support immune tolerance, or efficiently deliver neuroprotective factors in brain diseases in which current therapeutic options are very limited. In this article, we illustrate prospects and bottlenecks for the clinical development and implementation of engineered cellular immunotherapies in neurologic diseases.
MeSH term(s)	Humans ; Artificial Cells ; Nervous System Diseases/therapy ; Immunotherapy ; Brain Diseases ; Autoantibodies
Chemical Substances	Autoantibodies
Language	English
Publishing date	2023-06-29
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2767740-0
ISSN	2332-7812 ; 2332-7812
ISSN (online)	2332-7812
ISSN	2332-7812
DOI	10.1212/NXI.0000000000200139
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Article ; Online: Impact of complement activation on clinical outcomes in multiple sclerosis.

Keller, Christian W / Oechtering, Johanna / Wiendl, Heinz / Kappos, Ludwig / Kuhle, Jens / Lünemann, Jan D

Annals of clinical and translational neurology

2021 Volume 8, Issue 4, Page(s) 944–950

Abstract: We determined activation profiles of the classical and alternative complement pathway in 39 treatment-naïve patients with early relapse-onset MS. Plasma concentrations of complement fragments were unchanged in MS compared to 32 patients with non- ... ...

Abstract	We determined activation profiles of the classical and alternative complement pathway in 39 treatment-naïve patients with early relapse-onset MS. Plasma concentrations of complement fragments were unchanged in MS compared to 32 patients with non-inflammatory neurological diseases. Profiles in patients experiencing clinical exacerbations did not differ from patients with stable disease and did not correlate with baseline EDSS, numbers of T2 lesions and time to second relapse. Long-term EDSS outcomes 4 years after diagnosis did not significantly correlate with baseline complement levels. These data do not support the use of complement activation products as biomarkers for disease activity in early MS.
MeSH term(s)	Adult ; Biomarkers/blood ; Complement Activation/immunology ; Complement System Proteins/metabolism ; Cross-Sectional Studies ; Female ; Follow-Up Studies ; Humans ; Male ; Middle Aged ; Multiple Sclerosis, Relapsing-Remitting/blood ; Multiple Sclerosis, Relapsing-Remitting/immunology ; Multiple Sclerosis, Relapsing-Remitting/pathology ; Multiple Sclerosis, Relapsing-Remitting/physiopathology
Chemical Substances	Biomarkers ; Complement System Proteins (9007-36-7)
Language	English
Publishing date	2021-03-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2740696-9
ISSN	2328-9503 ; 2328-9503
ISSN (online)	2328-9503
ISSN	2328-9503
DOI	10.1002/acn3.51334
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Article ; Online: Antibody response to herpes simplex virus-1 is increased in autoimmune encephalitis.

Chuquisana, Omar / Strippel, Christine / Gross, Catharina C / Melzer, Nico / Kühn, Joachim / Kovac, Stjepana / Wiendl, Heinz / Lünemann, Jan D

European journal of immunology

2022 Volume 52, Issue 7, Page(s) 1198–1200

MeSH term(s)	Antibody Formation ; Encephalitis ; Hashimoto Disease ; Herpesvirus 1, Human ; Humans
Language	English
Publishing date	2022-04-27
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.202249854
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Article ; Online: Tracking the Electron Transfer Cascade in European Robin Cryptochrome 4 Mutants.

Timmer, Daniel / Frederiksen, Anders / Lünemann, Daniel C / Thomas, Anitta R / Xu, Jingjing / Bartölke, Rabea / Schmidt, Jessica / Kubař, Tomáš / De Sio, Antonietta / Solov'yov, Ilia A / Mouritsen, Henrik / Lienau, Christoph

Journal of the American Chemical Society

2023 Volume 145, Issue 21, Page(s) 11566–11578

Abstract: The primary step in the mechanism by which migratory birds sense the Earth's magnetic field is thought to be the light-induced formation of long-lived magnetically sensitive radical pairs within cryptochrome flavoproteins located in the birds' retinas. ... ...

Abstract	The primary step in the mechanism by which migratory birds sense the Earth's magnetic field is thought to be the light-induced formation of long-lived magnetically sensitive radical pairs within cryptochrome flavoproteins located in the birds' retinas. Blue-light absorption by the non-covalently bound flavin chromophore triggers sequential electron transfers along a chain of four tryptophan residues toward the photoexcited flavin. The recently demonstrated ability to express cryptochrome 4a from the night-migratory European robin (
MeSH term(s)	Cryptochromes/chemistry ; Tryptophan/chemistry ; Electrons ; Electron Transport ; Magnetic Fields ; Flavins/metabolism
Chemical Substances	Cryptochromes ; Tryptophan (8DUH1N11BX) ; Flavins
Language	English
Publishing date	2023-05-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3155-0
ISSN	1520-5126 ; 0002-7863
ISSN (online)	1520-5126
ISSN	0002-7863
DOI	10.1021/jacs.3c00442
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Article: Immune and myodegenerative pathomechanisms in inclusion body myositis.

Keller, Christian W / Schmidt, Jens / Lünemann, Jan D

Annals of clinical and translational neurology

2017 Volume 4, Issue 6, Page(s) 422–445

Abstract: Inclusion Body Myositis (IBM) is a relatively common acquired inflammatory myopathy in patients above 50 years of age. Pathological hallmarks of IBM are intramyofiber protein inclusions and endomysial inflammation, indicating that both myodegenerative ... ...

Abstract	Inclusion Body Myositis (IBM) is a relatively common acquired inflammatory myopathy in patients above 50 years of age. Pathological hallmarks of IBM are intramyofiber protein inclusions and endomysial inflammation, indicating that both myodegenerative and inflammatory mechanisms contribute to its pathogenesis. Impaired protein degradation by the autophagic machinery, which regulates innate and adaptive immune responses, in skeletal muscle fibers has recently been identified as a potential key pathomechanism in IBM. Immunotherapies, which are successfully used for treating other inflammatory myopathies lack efficacy in IBM and so far no effective treatment is available. Thus, a better understanding of the mechanistic pathways underlying progressive muscle weakness and atrophy in IBM is crucial in identifying novel promising targets for therapeutic intervention. Here, we discuss recent insights into the pathomechanistic network of mutually dependent inflammatory and degenerative events during IBM.
Language	English
Publishing date	2017-05-16
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2740696-9
ISSN	2328-9503
ISSN	2328-9503
DOI	10.1002/acn3.419
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Article ; Online: Impaired B Cell Expression of the Inhibitory Fcγ Receptor IIB in Myasthenia Gravis.

Keller, Christian W / Chuquisana, Omar / Derdelinckx, Judith / Gross, Catharina C / Berger, Klaus / Robinson, James / Nimmerjahn, Falk / Wiendl, Heinz / Willcox, Nick / Lünemann, Jan D

Annals of neurology

2022 Volume 92, Issue 6, Page(s) 1046–1051

Abstract: Myasthenia gravis (MG) is an autoimmune disease in which pathogenic immunoglobulin G antibodies bind to acetylcholine receptors (or to functionally related molecules at the neuromuscular junction). B cell expression of the inhibitory immunoglobulin G ... ...

Abstract	Myasthenia gravis (MG) is an autoimmune disease in which pathogenic immunoglobulin G antibodies bind to acetylcholine receptors (or to functionally related molecules at the neuromuscular junction). B cell expression of the inhibitory immunoglobulin G receptor, Fc-gamma receptor (FcγR) IIB, maintains peripheral immune tolerance, and its absence renders B cells hyperresponsive to autoantigen. Here, we report that FcγRIIB expression levels are substantially reduced in B lineage cells derived from immunotherapy-naïve patients with acetylcholine receptor antibody-positive early-onset MG. In contrast, genetic variants associated with impaired FcγRIIB expression are not enriched in MG, indicating post-transcriptional dysregulation. FcγR-targeted therapies could have therapeutic benefits in MG. ANN NEUROL 2022;92:1046-1051.
MeSH term(s)	Humans ; Receptors, IgG/genetics ; Myasthenia Gravis/genetics ; Receptors, Cholinergic ; B-Lymphocytes ; Immunoglobulin G
Chemical Substances	Receptors, IgG ; Receptors, Cholinergic ; Immunoglobulin G
Language	English
Publishing date	2022-09-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	80362-5
ISSN	1531-8249 ; 0364-5134
ISSN (online)	1531-8249
ISSN	0364-5134
DOI	10.1002/ana.26507
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Article ; Online: Complement activation contributes to GAD antibody-associated encephalitis.

Chuquisana, Omar / Strippel, Christine / Tröscher, Anna M / Baumgartner, Tobias / Rácz, Attila / Keller, Christian W / Elger, Christian E / Melzer, Nico / Kovac, Stjepana / Wiendl, Heinz / Bauer, Jan / Lünemann, Jan D

Acta neuropathologica

2022 Volume 144, Issue 2, Page(s) 381–383

MeSH term(s)	Autoantibodies ; Complement Activation ; Encephalitis ; Humans
Chemical Substances	Autoantibodies
Language	English
Publishing date	2022-06-13
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1079-0
ISSN	1432-0533 ; 0001-6322
ISSN (online)	1432-0533
ISSN	0001-6322
DOI	10.1007/s00401-022-02448-x
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Article ; Online: Autophagy in CD4+ T-cell immunity and tolerance.

Lünemann, J D / Münz, C

Cell death and differentiation

2009 Volume 16, Issue 1, Page(s) 79–86

Abstract: Autophagy is a homeostatic process that enables eukaryotic cells to deliver cytoplasmic constituents for lysosomal degradation, to recycle nutrients and to survive during starvation. In addition to these primordial functions, autophagy has emerged as a ... ...

Abstract	Autophagy is a homeostatic process that enables eukaryotic cells to deliver cytoplasmic constituents for lysosomal degradation, to recycle nutrients and to survive during starvation. In addition to these primordial functions, autophagy has emerged as a key mechanism in orchestrating innate and adaptive immune responses to intracellular pathogens. Autophagy restricts viral infections as well as replication of intracellular bacteria and parasites and delivers pathogenic determinants for TLR stimulation and for MHC class II presentation to the adaptive immune system. Apart from its role in defense against pathogens, autophagy-mediated presentation of self-antigens in the steady state could have a crucial role in the induction and maintenance of CD4(+) T-cell tolerance. This review describes the mechanisms by which the immune system utilizes autophagic degradation of cytoplasmic material to regulate adaptive immune responses.
MeSH term(s)	Animals ; Antigen Presentation ; Autoantigens/immunology ; Autophagy/immunology ; Bacteria/immunology ; Bacterial Infections/immunology ; CD4-Positive T-Lymphocytes/immunology ; Humans ; Immune Tolerance ; Immunity, Cellular ; Immunity, Innate ; Lysosomes/immunology ; Starvation/immunology ; Virus Diseases/immunology ; Viruses/immunology
Chemical Substances	Autoantigens
Language	English
Publishing date	2009-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1225672-9
ISSN	1476-5403 ; 1350-9047
ISSN (online)	1476-5403
ISSN	1350-9047
DOI	10.1038/cdd.2008.113
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Article ; Online: Reduced frequency of cytotoxic CD56

Pánisová, Elena / Lünemann, Anna / Bürgler, Simone / Kotur, Monika / Lazarovici, Julien / Danu, Alina / Kaulfuss, Meike / Mietz, Juliane / Chijioke, Obinna / Münz, Christian / Busson, Pierre / Berger, Christoph / Ghez, David / Azzi, Tarik

Cancer immunology, immunotherapy : CII

2021 Volume 71, Issue 1, Page(s) 13–24

Abstract: Around 30-50% of classical Hodgkin lymphoma (cHL) cases in immunocompetent individuals from industrialized countries are associated with the B-lymphotropic Epstein-Barr virus (EBV). Although natural killer (NK) cells exhibit anti-viral and anti-tumoral ... ...

Abstract	Around 30-50% of classical Hodgkin lymphoma (cHL) cases in immunocompetent individuals from industrialized countries are associated with the B-lymphotropic Epstein-Barr virus (EBV). Although natural killer (NK) cells exhibit anti-viral and anti-tumoral functions, virtually nothing is known about quantitative and qualitative differences in NK cells in patients with EBV+ cHL vs. EBV- cHL. Here, we prospectively investigated 36 cHL patients without known immune suppression or overt immunodeficiency at diagnosis. All 10 EBV+ cHL patients and 25 out 26 EBV- cHL were seropositive for EBV antibodies, and EBV+ cHL patients presented with higher plasma EBV DNA levels compared to EBV- cHL patients. We show that the CD56
MeSH term(s)	Adult ; Aged ; Antibodies/immunology ; Antineoplastic Agents/pharmacology ; CD56 Antigen/biosynthesis ; Epstein-Barr Virus Infections/complications ; Female ; GPI-Linked Proteins/biosynthesis ; Herpesvirus 4, Human/metabolism ; Hodgkin Disease/complications ; Hodgkin Disease/metabolism ; Hodgkin Disease/therapy ; Humans ; Immunotherapy ; In Vitro Techniques ; Killer Cells, Natural/metabolism ; Leukocytes, Mononuclear/cytology ; Lymphocytes/metabolism ; Lysosomal-Associated Membrane Protein 1/biosynthesis ; Male ; Middle Aged ; Phenotype ; Prospective Studies ; Receptors, IgG/biosynthesis ; Rituximab/pharmacology
Chemical Substances	Antibodies ; Antineoplastic Agents ; CD56 Antigen ; FCGR3B protein, human ; GPI-Linked Proteins ; Lysosomal-Associated Membrane Protein 1 ; NCAM1 protein, human ; Receptors, IgG ; Rituximab (4F4X42SYQ6)
Language	English
Publishing date	2021-05-15
Publishing country	Germany
Document type	Journal Article
ZDB-ID	195342-4
ISSN	1432-0851 ; 0340-7004
ISSN (online)	1432-0851
ISSN	0340-7004
DOI	10.1007/s00262-021-02956-x
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Article: Single-cell profiling reveals preferential reduction of memory B cell subsets in cladribine patients that correlates with treatment response.

Teschner, Valerie E / Fleck, Ann-Katrin / Walter, Carolin / Schwarze, Anna-Sophie / Eschborn, Melanie / Wirth, Timo / Steinberg, Olga V / Schulte-Mecklenbeck, Andreas / Lu, I-Na / Herrera-Rivero, Marisol / Janoschka, Claudia / Lünemann, Jan D / Schwab, Nicholas / Meyer Zu Hörste, Gerd / Varghese, Julian / Gross, Catharina C / Pul, Refik / Kleinschnitz, Christoph / Mader, Simone /

Meinl, Edgar / Stoll, Monika / Wiendl, Heinz / Klotz, Luisa

Therapeutic advances in neurological disorders

2023 Volume 16, Page(s) 17562864231211077

Abstract: Background: Cladribine is a highly effective immunotherapy that is applied in two short-term courses over 2 years and reduces relapse rate and disease progression in patients with relapsing multiple sclerosis (MS). Despite the short treatment period, ... ...

Abstract	Background: Cladribine is a highly effective immunotherapy that is applied in two short-term courses over 2 years and reduces relapse rate and disease progression in patients with relapsing multiple sclerosis (MS). Despite the short treatment period, cladribine has a long-lasting effect on disease activity even after recovery of lymphocyte counts, suggesting a yet undefined long-term immune modulating effect. Objectives: Our aim was to provide a more profound understanding of the detailed effects of cladribine, also with regard to the patients' therapy response. Design: We performed an open-labeled, explorative, prospective, single-arm study, in which we examined the detailed lymphocyte subset development of MS patients who received cladribine treatment over 2 years. Methods: We performed in-depth profiling of the effects of cladribine on peripheral blood lymphocytes by flow cytometry, bulk RNA sequencing of sorted CD4 Results: Flow cytometry revealed a predominant and sustained reduction of memory B cells compared to other B cell subsets after cladribine treatment, whereas T cell subsets were slightly reduced in a more uniform pattern. The overall transcriptional profile of total blood B cells exhibited reduced expression of proinflammatory and T cell activating genes, while single-cell transcriptomics revealed that gene expression within each B cell cluster did not change over time. Stable patients displayed stronger reductions of selected memory B cell clusters as compared to patients with clinical or cerebral MRI disease activity. Conclusion: We describe a pronounced and sustained effect of cladribine on the memory B cell compartment, and the resulting change in B cell subset composition causes a significant alteration of B cell transcriptional profiles resulting in reduced proinflammatory and T cell activating capacities. The extent of reduction in selected memory B cell clusters by cladribine may predict treatment response.
Language	English
Publishing date	2023-12-09
Publishing country	England
Document type	Journal Article
ZDB-ID	2442245-9
ISSN	1756-2864 ; 1756-2856
ISSN (online)	1756-2864
ISSN	1756-2856
DOI	10.1177/17562864231211077
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