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9 results on '"Lünemann, J.D."'

2. Multiple Sclerosis Therapy Consensus Group (MSTCG): position statement on disease-modifying therapies for multiple sclerosis (white paper)

Author

Wiendl, H., Gold, R., Berger, T., Derfuss, T., Linker, R., Mäurer, M., Aktas, O., Baum, K., Berghoff, M., Bittner, S., Chan, A., Czaplinski, A., Deisenhammer, F., Di Pauli, F., Du Pasquier, R., Enzinger, C., Fertl, E., Gass, A., Gehring, K., Gobbi, C., Goebels, N., Guger, M., Haghikia, A., Hartung, H.P., Heidenreich, F., Hoffmann, O., Kallmann, B., Kleinschnitz, C., Klotz, L., Leussink, V.I., Leutmezer, F., Limmroth, V., Lünemann, J.D., Lutterotti, A., Meuth, S.G., Meyding-Lamadé, U., Platten, M., Rieckmann, P., Schmidt, S., Tumani, H., Weber, F., Weber, M.S., Zettl, U.K., Ziemssen, T., Zipp, F., and ‘Multiple Sclerosis Therapy Consensus Group' (MSTCG)

Subjects
disease-modifying therapy, guideline, multiple sclerosis, treatment recommendation
Abstract

Multiple sclerosis is a complex, autoimmune-mediated disease of the central nervous system characterized by inflammatory demyelination and axonal/neuronal damage. The approval of various disease-modifying therapies and our increased understanding of disease mechanisms and evolution in recent years have significantly changed the prognosis and course of the disease. This update of the Multiple Sclerosis Therapy Consensus Group treatment recommendation focuses on the most important recommendations for disease-modifying therapies of multiple sclerosis in 2021. Our recommendations are based on current scientific evidence and apply to those medications approved in wide parts of Europe, particularly German-speaking countries (Germany, Austria, and Switzerland).

Published
2021

3. NLRP3 inflammasome as prognostic factor and therapeutic target in primary progressive multiple sclerosis patients

Author

Malhotra, S., Costa, C., Eixarch, H., Keller, C.W., Amman, L., Martínez-Banaclocha, H., Midaglia, L., Sarró, E., Machín-Díaz, Isabel, Villar, L.M., Triviño, J.C., Oliver-Martos, Begoña, Parladé, L.N., Calvo-Barreiro, L., Matesanz, F., Vandenbroeck, K., Urcelay, E., Martínez-Ginés, M.L., Tejeda-Velarde, A., Fissolo, N., Castilló, J., Sanchez, A., Robertson, A.A.B., Clemente, Diego, Prinz, M., Pelegrín, Pablo, Lünemann, J.D., Espejo, C., Montalbán, Xavier, Comabella, Manuel, Malhotra, S., Costa, C., Eixarch, H., Keller, C.W., Amman, L., Martínez-Banaclocha, H., Midaglia, L., Sarró, E., Machín-Díaz, Isabel, Villar, L.M., Triviño, J.C., Oliver-Martos, Begoña, Parladé, L.N., Calvo-Barreiro, L., Matesanz, F., Vandenbroeck, K., Urcelay, E., Martínez-Ginés, M.L., Tejeda-Velarde, A., Fissolo, N., Castilló, J., Sanchez, A., Robertson, A.A.B., Clemente, Diego, Prinz, M., Pelegrín, Pablo, Lünemann, J.D., Espejo, C., Montalbán, Xavier, and Comabella, Manuel

Abstract

Primary progressive multiple sclerosis is a poorly understood disease entity with no specific prognostic biomarkers and scarce therapeutic options. We aimed to identify disease activity biomarkers in multiple sclerosis by performing an RNA sequencing approach in peripheral blood mononuclear cells from a discovery cohort of 44 untreated patients with multiple sclerosis belonging to different clinical forms and activity phases of the disease, and 12 healthy control subjects. A validation cohort of 58 patients with multiple sclerosis and 26 healthy control subjects was included in the study to replicate the RNA sequencing findings. The RNA sequencing revealed an interleukin 1 beta (IL1B) signature in patients with primary progressive multiple sclerosis. Subsequent immunophenotyping pointed to blood monocytes as responsible for the IL1B signature observed in this group of patients. Functional experiments at baseline measuring apoptosis-associated speck-like protein containing a CARD (ASC) speck formation showed that the NOD-leucine rich repeat and pyrin containing protein 3 (NLRP3) inflammasome was overactive in monocytes from patients with primary progressive multiple sclerosis, and canonical NLRP3 inflammasome activation with a combination of ATP plus lipopolysaccharide was associated with increased IL1B production in this group of patients. Primary progressive multiple sclerosis patients with high IL1B gene expression levels in peripheral blood mononuclear cells progressed significantly faster compared to patients with low IL1B levels based on the time to reach an EDSS of 6.0 and the Multiple Sclerosis Severity Score. In agreement with peripheral blood findings, both NLRP3 and IL1B expression in brain tissue from patients with primary progressive multiple sclerosis was mainly restricted to cells of myeloid lineage. Treatment of mice with a specific NLRP3 inflammasome inhibitor attenuated established experimental autoimmune encephalomyelitis disease severity and impro

Published
2020

4. IVIG efficacy in CIDP patients is not associated with terminal complement inhibition

Author

Keller, C.W. Quast, I. Dalakas, M.C. Lünemann, J.D.

Abstract

Patients with acute and chronic inflammatory demyelinating neuropathies exhibit elevated serum and cerebrospinal fluid (CSF) levels of terminal complement activation products and therapeutic inhibition of complement activation is currently tested for its safety and efficacy in patients with Guillain-Barré syndrome (GBS). Here, we determined serum levels of the complement activation products C3a, C5a and the soluble terminal complement complex (sTCC) in 39 individuals with chronic inflammatory demyelinating polyneuropathy (CIDP) who participated in one of the largest ever conducted clinical trial in patients with CIDP (ICE trial) and received Intravenous Immunoglobulin (IVIG) or placebo (albumin) in 3 week intervals for up to 24 weeks. In placebo-treated patients with spontaneous disease remission, serum sTCC levels moderately decreased over time. Levels of complement activation products were, however, not modulated by IVIG and remained unchanged in patients with a beneficial response to IVIG therapy as compared to those with steady or worsened disease. These results suggest that the therapeutic efficacy of IVIG in CIDP is based on immunomodulatory mechanisms different from complement inhibition. Terminal complement activation merits further investigation as a surrogate marker for disease progression and therapeutic target in patients with CIDP. © 2019 Elsevier B.V.

Published
2019

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