MIF in the cerebrospinal fluid is decreased during relapsing-remitting while increased in secondary progressive multiple sclerosis
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Macrophage migration inhibitory factor (MIF) is involved in the function of both the innate and adaptive immune systems and in neuroprotection and has recently been implicated in multiple sclerosis (MS).
Objectives
Determination of MIF levels in the cerebrospinal fluid (CSF) of patients with distinct subtypes of MS and the cellular localization of MIF in human brain tissue.
Methods
The levels of MIF were investigated in CSF from patients with clinically isolated syndrome (CIS) (n = 26), relapsing-remitting MS (RRMS) (n = 22), secondary progressive MS (SPMS) (n = 19), and healthy controls (HCs) (n = 24), using ELISA. The effect of disease-modifying therapies in the RRMS and SPMS cohorts were examined. Cellular distribution of MIF in the human brain was studied using immunochemistry and the newly available OligoInternode database.
Results
MIF was significantly decreased in treatment-naïve CIS and RRMS patients compared to HCs but was elevated in SPMS. Interestingly, MIF levels were sex-dependent and significantly lower in women with CIS and RRMS. MIF expression in the human brain was localized to neurons, astrocytes, pericytes, and oligo5 oligodendrocytes but not in microglia.
Conclusion
The finding that MIF was decreased in newly diagnosed CIS and RRMS patients but was high in patients with SPMS may suggest that MIF levels in CSF are regulated by local MIF receptor expression that affects the overall MIF signaling in the brain and may represent a protective mechanism that eventually fails.
| Originalsprog | Engelsk |
|---|---|
| Artikelnummer | 120320 |
| Tidsskrift | Journal of the Neurological Sciences |
| Vol/bind | 439 |
| Antal sider | 13 |
| ISSN | 0022-510X |
| DOI | |
| Status | Udgivet - 2022 |
Bibliografisk note
Funding Information:
This work was supported by: Jaschafonden, Scleroseforeningen, Hans og Oda Svenningsens Fond, Aage og Johanne Louis-Hansens Fond, Knut og Edith Eriksens Mindefond, Kong Christians den Tiendes Fond, Direktør Ejnar Jonasson, kaldet Johnsen og Hustru's Mindelegat, Trigon Fonden. The Swedish Multiple Sclerosis Research Foundation, the Swedish Federal Government (LUA/ALF Agreement ALFGBG-722081 ), the Swedish Association of Persons with Neurological Disabilities, the Research Foundation of the Multiple Sclerosis Society of Gothenburg, the Edit Jacobson Foundation, and NEURO Sweden.
Funding Information:
This work was supported by: Jaschafonden, Scleroseforeningen, Hans og Oda Svenningsens Fond, Aage og Johanne Louis-Hansens Fond, Knut og Edith Eriksens Mindefond, Kong Christians den Tiendes Fond, Direktør Ejnar Jonasson, kaldet Johnsen og Hustru's Mindelegat, Trigon Fonden. The Swedish Multiple Sclerosis Research Foundation, the Swedish Federal Government (LUA/ALF Agreement ALFGBG-722081), the Swedish Association of Persons with Neurological Disabilities, the Research Foundation of the Multiple Sclerosis Society of Gothenburg, the Edit Jacobson Foundation, and NEURO Sweden.ZI has served on scientific advisory boards as consultant and received support for congress participation, speaker honoraria, and honoraria as a member of the Clinical Endpoint Committee for phase 3 medical trials, and has received research support from Biogen, Merck-Serono, Sanofi-Genzyme, Novartis, Roche, Bristol-Myers-Squibb, Alexion, and Lundbeckfonden.
Publisher Copyright:
© 2022 Elsevier B.V.
ID: 345501268