Evidence map›Paper›PMID 42802280›Full record

ArticleJournal of neurology2026

The role of leukocyte p38 MAP kinase in immune-mediated peripheral polyneuropathies: distinct modulation by intravenous immunoglobulins.

Marina Stamenkovic, Irena Vukovic, Emina Milosevic, Stojan Peric, Aleksandar Paunic, Aleksandra Anicin, Ivana Basta, Ivo Bozovic, Aleksa Palibrk, Vukan Ivanovic and 2 more

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Article in Journal of neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

12 authors.

Marina Stamenkovic *Institute of Microbiology and Immunology, Faculty of Medicine, University of Belgrade, Belgrade, Serbia.
Irena Vukovic *Institute of Microbiology and Immunology, Faculty of Medicine, University of Belgrade, Belgrade, Serbia.
Emina MilosevicInstitute of Microbiology and Immunology, Faculty of Medicine, University of Belgrade, Belgrade, Serbia.
Stojan PericFaculty of Medicine, Neurology Clinic, University Clinical Centre of Serbia, University of Belgrade, Belgrade, Serbia.
Aleksandar PaunicInstitute of Microbiology and Immunology, Faculty of Medicine, University of Belgrade, Belgrade, Serbia.
Aleksandra AnicinInstitute of Microbiology and Immunology, Faculty of Medicine, University of Belgrade, Belgrade, Serbia.
Ivana BastaFaculty of Medicine, Neurology Clinic, University Clinical Centre of Serbia, University of Belgrade, Belgrade, Serbia.
Ivo BozovicFaculty of Medicine, Neurology Clinic, University Clinical Centre of Serbia, University of Belgrade, Belgrade, Serbia.
Aleksa PalibrkFaculty of Medicine, Neurology Clinic, University Clinical Centre of Serbia, University of Belgrade, Belgrade, Serbia.
Vukan IvanovicFaculty of Medicine, Neurology Clinic, University Clinical Centre of Serbia, University of Belgrade, Belgrade, Serbia.
Vladimir TrajkovicInstitute of Microbiology and Immunology, Faculty of Medicine, University of Belgrade, Belgrade, Serbia.
Verica PaunovicInstitute of Microbiology and Immunology, Faculty of Medicine, University of Belgrade, Belgrade, Serbia. verica.paunovic@med.bg.ac.rs.ORCID http://orcid.org/0000-0002-4912-7761

Funding

Ministarstvo Prosvete, Nauke i Tehnološkog Razvoja 451-03-47/2022-01/200110Ministarstvo Prosvete, Nauke i Tehnološkog Razvoja 451-03-47/2023-01/200110Ministarstvo Prosvete, Nauke i Tehnološkog Razvoja 451-03-66/2024-03/200110Ministarstvo Prosvete, Nauke i Tehnološkog Razvoja 451-03-9/2021-14/200110
6 · The paper itself

Abstract

backgroundChronic inflammatory demyelinating polyneuropathy (CIDP) and multifocal motor neuropathy (MMN) are rare immune-mediated peripheral polyneuropathies with insufficiently elucidated etiopathogenesis. Mitogen activated protein kinases (MAPK), the intracellular energy sensor AMP-activated protein kinase (AMPK), and the master metabolic regulator mechanistic target of rapamycin complex 1 (mTORC1) regulate immune responses through various mechanisms, including autophagy.

methodsWe used immunoblotting to analyze AMPK/mTORC1 signaling, autophagy, and the activation status of the MAPK family members p38, extracellular signal-regulated protein kinase (ERK), and c-Jun N-terminal kinase (JNK) in peripheral blood mononuclear cells (PBMC) of 17 treatment-naïve CIDP patients and 7 MMN patients already on chronic intravenous immunoglobulin (IVIg) therapy.

resultsCompared with age/sex-matched controls, PBMC from CIDP and MMN patients showed higher levels of active (phosphorylated) p38 MAPK, whereas autophagy and AMPK/mTORC1, ERK, and JNK pathways were not significantly altered. The amounts of p38 MAPK in PBMC negatively correlated with muscle strength in MMN, but not CIDP. The treatment of CIDP patients (n = 9) with IVIg did not affect the activation status of AMPK, MAPK, or autophagy in PBMC. In contrast, IVIg treatment reduced the phosphorylation of p38 MAPK, ERK, and AMPK in PBMC from MMN patients (n = 6), and the decrease in phospho-p38 MAPK levels correlated with improved hand grip strength.

conclusionsTogether, this exploratory study indicates that leukocyte p38 MAPK modulation might be involved in disease activity and therapeutic effect of IVIg in MMN, but not CIDP.

Indexed as

Immunoglobulins, IntravenousImmunologic FactorsLeukocytes, Mononuclearp38 Mitogen-Activated Protein KinasesPolyneuropathiesPolyradiculoneuropathy, Chronic Inflammatory DemyelinatingAdultAgedAutophagyFemaleHumansMaleMechanistic Target of Rapamycin Complex 1Middle AgedImmunoglobulins, IntravenousImmunologic FactorsMechanistic Target of Rapamycin Complex 1p38 Mitogen-Activated Protein KinasesCIDPIVIgMMNp38 MAPKPeripheral polyneuropathies

Identifiers

PMID42802280

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.