Immune cell modulation of oligodendrocyte lineage cells

Chronic demyelination and the concomitant loss of trophic support and increased energy demands in axons are thought to contribute to neurodegeneration in a number of neurological diseases such as multiple sclerosis (MS). Adult oligodendrocyte precursor cells (OPCs) play an important role in these de...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Harrington, Emily P. [verfasserIn] Bergles, Dwight E. [verfasserIn] Calabresi, Peter A. [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2019

Schlagwörter:	Oligodendrocytes Multiple sclerosis Remyelination Myelin repair Antigen presentation CD8 T cells

Übergeordnetes Werk:	Enthalten in: Neuroscience letters - Amsterdam [u.a.] : Elsevier Science, 1975, 715
Übergeordnetes Werk:	volume:715

DOI / URN:	10.1016/j.neulet.2019.134601

Katalog-ID:	ELV003317064

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520			\|a Chronic demyelination and the concomitant loss of trophic support and increased energy demands in axons are thought to contribute to neurodegeneration in a number of neurological diseases such as multiple sclerosis (MS). Adult oligodendrocyte precursor cells (OPCs) play an important role in these demyelinating diseases by generating new myelinating oligodendrocytes that may help limit axonal degeneration. Thus, promoting the differentiation of OPCs and functional integration of newly generated oligodendrocytes is a crucial avenue for the next generation of therapies. Evidence to date suggests that the immune system may both positively and negatively impact OPC differentiation and endogenous remyelination in disease. Inflammatory cytokines not only suppress OPC differentiation but may also directly affect other functions of OPCs. Recent studies have demonstrated that OPCs and oligodendrocytes in both human multiple sclerosis lesions and mouse models of demyelination can express an immunogenic transcriptional signature and upregulate antigen presenting genes. In inflammatory demyelinating mouse models OPCs are capable of presenting antigen and activating CD8 + T cells. Here we review the evidence for this new role of oligodendroglia as antigen presenting cells and how these inflammatory OPCs (iOPCs) and inflammatory oligodendrocytes (iOLs) may influence myelin repair and other disease processes.
650		4	\|a Oligodendrocytes
650		4	\|a Multiple sclerosis
650		4	\|a Remyelination
650		4	\|a Myelin repair
650		4	\|a Antigen presentation
650		4	\|a CD8 T cells
700	1		\|a Bergles, Dwight E. \|e verfasserin \|4 aut
700	1		\|a Calabresi, Peter A. \|e verfasserin \|0 (orcid)0000-0002-7776-6472 \|4 aut
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936	b	k	\|a 44.90 \|j Neurologie
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allfields	10.1016/j.neulet.2019.134601 doi (DE-627)ELV003317064 (ELSEVIER)S0304-3940(19)30704-9 DE-627 ger DE-627 rda eng 610 DE-600 44.90 bkl Harrington, Emily P. verfasserin (orcid)0000-0001-6352-8687 aut Immune cell modulation of oligodendrocyte lineage cells 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Chronic demyelination and the concomitant loss of trophic support and increased energy demands in axons are thought to contribute to neurodegeneration in a number of neurological diseases such as multiple sclerosis (MS). Adult oligodendrocyte precursor cells (OPCs) play an important role in these demyelinating diseases by generating new myelinating oligodendrocytes that may help limit axonal degeneration. Thus, promoting the differentiation of OPCs and functional integration of newly generated oligodendrocytes is a crucial avenue for the next generation of therapies. Evidence to date suggests that the immune system may both positively and negatively impact OPC differentiation and endogenous remyelination in disease. Inflammatory cytokines not only suppress OPC differentiation but may also directly affect other functions of OPCs. Recent studies have demonstrated that OPCs and oligodendrocytes in both human multiple sclerosis lesions and mouse models of demyelination can express an immunogenic transcriptional signature and upregulate antigen presenting genes. In inflammatory demyelinating mouse models OPCs are capable of presenting antigen and activating CD8 + T cells. Here we review the evidence for this new role of oligodendroglia as antigen presenting cells and how these inflammatory OPCs (iOPCs) and inflammatory oligodendrocytes (iOLs) may influence myelin repair and other disease processes. Oligodendrocytes Multiple sclerosis Remyelination Myelin repair Antigen presentation CD8 T cells Bergles, Dwight E. verfasserin aut Calabresi, Peter A. verfasserin (orcid)0000-0002-7776-6472 aut Enthalten in Neuroscience letters Amsterdam [u.a.] : Elsevier Science, 1975 715 Online-Ressource (DE-627)306589699 (DE-600)1498535-4 (DE-576)081953119 1872-7972 nnns volume:715 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2336 GBV_ILN_2522 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 44.90 Neurologie AR 715
spelling	10.1016/j.neulet.2019.134601 doi (DE-627)ELV003317064 (ELSEVIER)S0304-3940(19)30704-9 DE-627 ger DE-627 rda eng 610 DE-600 44.90 bkl Harrington, Emily P. verfasserin (orcid)0000-0001-6352-8687 aut Immune cell modulation of oligodendrocyte lineage cells 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Chronic demyelination and the concomitant loss of trophic support and increased energy demands in axons are thought to contribute to neurodegeneration in a number of neurological diseases such as multiple sclerosis (MS). Adult oligodendrocyte precursor cells (OPCs) play an important role in these demyelinating diseases by generating new myelinating oligodendrocytes that may help limit axonal degeneration. Thus, promoting the differentiation of OPCs and functional integration of newly generated oligodendrocytes is a crucial avenue for the next generation of therapies. Evidence to date suggests that the immune system may both positively and negatively impact OPC differentiation and endogenous remyelination in disease. Inflammatory cytokines not only suppress OPC differentiation but may also directly affect other functions of OPCs. Recent studies have demonstrated that OPCs and oligodendrocytes in both human multiple sclerosis lesions and mouse models of demyelination can express an immunogenic transcriptional signature and upregulate antigen presenting genes. In inflammatory demyelinating mouse models OPCs are capable of presenting antigen and activating CD8 + T cells. Here we review the evidence for this new role of oligodendroglia as antigen presenting cells and how these inflammatory OPCs (iOPCs) and inflammatory oligodendrocytes (iOLs) may influence myelin repair and other disease processes. Oligodendrocytes Multiple sclerosis Remyelination Myelin repair Antigen presentation CD8 T cells Bergles, Dwight E. verfasserin aut Calabresi, Peter A. verfasserin (orcid)0000-0002-7776-6472 aut Enthalten in Neuroscience letters Amsterdam [u.a.] : Elsevier Science, 1975 715 Online-Ressource (DE-627)306589699 (DE-600)1498535-4 (DE-576)081953119 1872-7972 nnns volume:715 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2336 GBV_ILN_2522 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 44.90 Neurologie AR 715
allfields_unstemmed	10.1016/j.neulet.2019.134601 doi (DE-627)ELV003317064 (ELSEVIER)S0304-3940(19)30704-9 DE-627 ger DE-627 rda eng 610 DE-600 44.90 bkl Harrington, Emily P. verfasserin (orcid)0000-0001-6352-8687 aut Immune cell modulation of oligodendrocyte lineage cells 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Chronic demyelination and the concomitant loss of trophic support and increased energy demands in axons are thought to contribute to neurodegeneration in a number of neurological diseases such as multiple sclerosis (MS). Adult oligodendrocyte precursor cells (OPCs) play an important role in these demyelinating diseases by generating new myelinating oligodendrocytes that may help limit axonal degeneration. Thus, promoting the differentiation of OPCs and functional integration of newly generated oligodendrocytes is a crucial avenue for the next generation of therapies. Evidence to date suggests that the immune system may both positively and negatively impact OPC differentiation and endogenous remyelination in disease. Inflammatory cytokines not only suppress OPC differentiation but may also directly affect other functions of OPCs. Recent studies have demonstrated that OPCs and oligodendrocytes in both human multiple sclerosis lesions and mouse models of demyelination can express an immunogenic transcriptional signature and upregulate antigen presenting genes. In inflammatory demyelinating mouse models OPCs are capable of presenting antigen and activating CD8 + T cells. Here we review the evidence for this new role of oligodendroglia as antigen presenting cells and how these inflammatory OPCs (iOPCs) and inflammatory oligodendrocytes (iOLs) may influence myelin repair and other disease processes. Oligodendrocytes Multiple sclerosis Remyelination Myelin repair Antigen presentation CD8 T cells Bergles, Dwight E. verfasserin aut Calabresi, Peter A. verfasserin (orcid)0000-0002-7776-6472 aut Enthalten in Neuroscience letters Amsterdam [u.a.] : Elsevier Science, 1975 715 Online-Ressource (DE-627)306589699 (DE-600)1498535-4 (DE-576)081953119 1872-7972 nnns volume:715 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2336 GBV_ILN_2522 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 44.90 Neurologie AR 715
allfieldsGer	10.1016/j.neulet.2019.134601 doi (DE-627)ELV003317064 (ELSEVIER)S0304-3940(19)30704-9 DE-627 ger DE-627 rda eng 610 DE-600 44.90 bkl Harrington, Emily P. verfasserin (orcid)0000-0001-6352-8687 aut Immune cell modulation of oligodendrocyte lineage cells 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Chronic demyelination and the concomitant loss of trophic support and increased energy demands in axons are thought to contribute to neurodegeneration in a number of neurological diseases such as multiple sclerosis (MS). Adult oligodendrocyte precursor cells (OPCs) play an important role in these demyelinating diseases by generating new myelinating oligodendrocytes that may help limit axonal degeneration. Thus, promoting the differentiation of OPCs and functional integration of newly generated oligodendrocytes is a crucial avenue for the next generation of therapies. Evidence to date suggests that the immune system may both positively and negatively impact OPC differentiation and endogenous remyelination in disease. Inflammatory cytokines not only suppress OPC differentiation but may also directly affect other functions of OPCs. Recent studies have demonstrated that OPCs and oligodendrocytes in both human multiple sclerosis lesions and mouse models of demyelination can express an immunogenic transcriptional signature and upregulate antigen presenting genes. In inflammatory demyelinating mouse models OPCs are capable of presenting antigen and activating CD8 + T cells. Here we review the evidence for this new role of oligodendroglia as antigen presenting cells and how these inflammatory OPCs (iOPCs) and inflammatory oligodendrocytes (iOLs) may influence myelin repair and other disease processes. Oligodendrocytes Multiple sclerosis Remyelination Myelin repair Antigen presentation CD8 T cells Bergles, Dwight E. verfasserin aut Calabresi, Peter A. verfasserin (orcid)0000-0002-7776-6472 aut Enthalten in Neuroscience letters Amsterdam [u.a.] : Elsevier Science, 1975 715 Online-Ressource (DE-627)306589699 (DE-600)1498535-4 (DE-576)081953119 1872-7972 nnns volume:715 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2336 GBV_ILN_2522 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 44.90 Neurologie AR 715
allfieldsSound	10.1016/j.neulet.2019.134601 doi (DE-627)ELV003317064 (ELSEVIER)S0304-3940(19)30704-9 DE-627 ger DE-627 rda eng 610 DE-600 44.90 bkl Harrington, Emily P. verfasserin (orcid)0000-0001-6352-8687 aut Immune cell modulation of oligodendrocyte lineage cells 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Chronic demyelination and the concomitant loss of trophic support and increased energy demands in axons are thought to contribute to neurodegeneration in a number of neurological diseases such as multiple sclerosis (MS). Adult oligodendrocyte precursor cells (OPCs) play an important role in these demyelinating diseases by generating new myelinating oligodendrocytes that may help limit axonal degeneration. Thus, promoting the differentiation of OPCs and functional integration of newly generated oligodendrocytes is a crucial avenue for the next generation of therapies. Evidence to date suggests that the immune system may both positively and negatively impact OPC differentiation and endogenous remyelination in disease. Inflammatory cytokines not only suppress OPC differentiation but may also directly affect other functions of OPCs. Recent studies have demonstrated that OPCs and oligodendrocytes in both human multiple sclerosis lesions and mouse models of demyelination can express an immunogenic transcriptional signature and upregulate antigen presenting genes. In inflammatory demyelinating mouse models OPCs are capable of presenting antigen and activating CD8 + T cells. Here we review the evidence for this new role of oligodendroglia as antigen presenting cells and how these inflammatory OPCs (iOPCs) and inflammatory oligodendrocytes (iOLs) may influence myelin repair and other disease processes. Oligodendrocytes Multiple sclerosis Remyelination Myelin repair Antigen presentation CD8 T cells Bergles, Dwight E. verfasserin aut Calabresi, Peter A. verfasserin (orcid)0000-0002-7776-6472 aut Enthalten in Neuroscience letters Amsterdam [u.a.] : Elsevier Science, 1975 715 Online-Ressource (DE-627)306589699 (DE-600)1498535-4 (DE-576)081953119 1872-7972 nnns volume:715 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2336 GBV_ILN_2522 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 44.90 Neurologie AR 715
language	English
source	Enthalten in Neuroscience letters 715 volume:715
sourceStr	Enthalten in Neuroscience letters 715 volume:715
format_phy_str_mv	Article
bklname	Neurologie
institution	findex.gbv.de
topic_facet	Oligodendrocytes Multiple sclerosis Remyelination Myelin repair Antigen presentation CD8 T cells
dewey-raw	610
isfreeaccess_bool	false
container_title	Neuroscience letters
authorswithroles_txt_mv	Harrington, Emily P. @@aut@@ Bergles, Dwight E. @@aut@@ Calabresi, Peter A. @@aut@@
publishDateDaySort_date	2019-01-01T00:00:00Z
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author	Harrington, Emily P.
spellingShingle	Harrington, Emily P. ddc 610 bkl 44.90 misc Oligodendrocytes misc Multiple sclerosis misc Remyelination misc Myelin repair misc Antigen presentation misc CD8 T cells Immune cell modulation of oligodendrocyte lineage cells
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topic	ddc 610 bkl 44.90 misc Oligodendrocytes misc Multiple sclerosis misc Remyelination misc Myelin repair misc Antigen presentation misc CD8 T cells
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title	Immune cell modulation of oligodendrocyte lineage cells
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title_sort	immune cell modulation of oligodendrocyte lineage cells
title_auth	Immune cell modulation of oligodendrocyte lineage cells
abstract	Chronic demyelination and the concomitant loss of trophic support and increased energy demands in axons are thought to contribute to neurodegeneration in a number of neurological diseases such as multiple sclerosis (MS). Adult oligodendrocyte precursor cells (OPCs) play an important role in these demyelinating diseases by generating new myelinating oligodendrocytes that may help limit axonal degeneration. Thus, promoting the differentiation of OPCs and functional integration of newly generated oligodendrocytes is a crucial avenue for the next generation of therapies. Evidence to date suggests that the immune system may both positively and negatively impact OPC differentiation and endogenous remyelination in disease. Inflammatory cytokines not only suppress OPC differentiation but may also directly affect other functions of OPCs. Recent studies have demonstrated that OPCs and oligodendrocytes in both human multiple sclerosis lesions and mouse models of demyelination can express an immunogenic transcriptional signature and upregulate antigen presenting genes. In inflammatory demyelinating mouse models OPCs are capable of presenting antigen and activating CD8 + T cells. Here we review the evidence for this new role of oligodendroglia as antigen presenting cells and how these inflammatory OPCs (iOPCs) and inflammatory oligodendrocytes (iOLs) may influence myelin repair and other disease processes.
abstractGer	Chronic demyelination and the concomitant loss of trophic support and increased energy demands in axons are thought to contribute to neurodegeneration in a number of neurological diseases such as multiple sclerosis (MS). Adult oligodendrocyte precursor cells (OPCs) play an important role in these demyelinating diseases by generating new myelinating oligodendrocytes that may help limit axonal degeneration. Thus, promoting the differentiation of OPCs and functional integration of newly generated oligodendrocytes is a crucial avenue for the next generation of therapies. Evidence to date suggests that the immune system may both positively and negatively impact OPC differentiation and endogenous remyelination in disease. Inflammatory cytokines not only suppress OPC differentiation but may also directly affect other functions of OPCs. Recent studies have demonstrated that OPCs and oligodendrocytes in both human multiple sclerosis lesions and mouse models of demyelination can express an immunogenic transcriptional signature and upregulate antigen presenting genes. In inflammatory demyelinating mouse models OPCs are capable of presenting antigen and activating CD8 + T cells. Here we review the evidence for this new role of oligodendroglia as antigen presenting cells and how these inflammatory OPCs (iOPCs) and inflammatory oligodendrocytes (iOLs) may influence myelin repair and other disease processes.
abstract_unstemmed	Chronic demyelination and the concomitant loss of trophic support and increased energy demands in axons are thought to contribute to neurodegeneration in a number of neurological diseases such as multiple sclerosis (MS). Adult oligodendrocyte precursor cells (OPCs) play an important role in these demyelinating diseases by generating new myelinating oligodendrocytes that may help limit axonal degeneration. Thus, promoting the differentiation of OPCs and functional integration of newly generated oligodendrocytes is a crucial avenue for the next generation of therapies. Evidence to date suggests that the immune system may both positively and negatively impact OPC differentiation and endogenous remyelination in disease. Inflammatory cytokines not only suppress OPC differentiation but may also directly affect other functions of OPCs. Recent studies have demonstrated that OPCs and oligodendrocytes in both human multiple sclerosis lesions and mouse models of demyelination can express an immunogenic transcriptional signature and upregulate antigen presenting genes. In inflammatory demyelinating mouse models OPCs are capable of presenting antigen and activating CD8 + T cells. Here we review the evidence for this new role of oligodendroglia as antigen presenting cells and how these inflammatory OPCs (iOPCs) and inflammatory oligodendrocytes (iOLs) may influence myelin repair and other disease processes.
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title_short	Immune cell modulation of oligodendrocyte lineage cells
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up_date	2024-07-06T19:12:56.227Z
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Immune cell modulation of oligodendrocyte lineage cells

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