Contribution of LTi and T
Animals
B-Lymphocytes
/ immunology
Cell Aggregation
/ immunology
Central Nervous System
/ immunology
Disease Models, Animal
Encephalomyelitis, Autoimmune, Experimental
/ immunology
Female
Immunity, Innate
/ immunology
Lymphoid Tissue
/ immunology
Mice
Mice, Inbred C57BL
Multiple Sclerosis
/ immunology
Pregnancy
Th17 Cells
/ immunology
EAE
LTi cells
MP4
MS
TH17 cells
Journal
Journal of neuroinflammation
ISSN: 1742-2094
Titre abrégé: J Neuroinflammation
Pays: England
ID NLM: 101222974
Informations de publication
Date de publication:
28 May 2019
28 May 2019
Historique:
received:
29
11
2018
accepted:
06
05
2019
entrez:
30
5
2019
pubmed:
30
5
2019
medline:
25
12
2019
Statut:
epublish
Résumé
In a subgroup of patients suffering from progressive multiple sclerosis (MS), which is an inflammation-mediated neurodegenerative disease of the central nervous system (CNS), B cell aggregates were discovered within the meninges. Occurrence of these structures was associated with a more severe disease course and cortical histopathology. We have developed the B cell-dependent MP4-induced experimental autoimmune encephalomyelitis (EAE) as a mouse model to mimic this trait of the human disease. The aim of this study was to determine a potential role of lymphoid tissue inducer (LTi) and T We performed flow cytometry of cerebellar and splenic tissue of MP4-immunized mice in the acute and chronic stage of the disease to analyze the presence of CD3 While we were able to detect LTi cells in the embryonic spleen and adult intestine, which served as positive controls, there was no evidence for the existence of such a population in acute or chronic EAE in neither of the two models. Yet, we detected CD3 The absence of LTi cells in the cerebellum suggests that other cells might take over the function as an initiator of lymphoid tissue formation in the CNS. Overall, the development of ectopic lymphoid organs is a complex process based on an interplay between several molecules and signals. Here, we propose some potential candidates, which might be involved in the formation of B cell aggregates in the CNS of MP4-immunized mice.
Sections du résumé
BACKGROUND
BACKGROUND
In a subgroup of patients suffering from progressive multiple sclerosis (MS), which is an inflammation-mediated neurodegenerative disease of the central nervous system (CNS), B cell aggregates were discovered within the meninges. Occurrence of these structures was associated with a more severe disease course and cortical histopathology. We have developed the B cell-dependent MP4-induced experimental autoimmune encephalomyelitis (EAE) as a mouse model to mimic this trait of the human disease. The aim of this study was to determine a potential role of lymphoid tissue inducer (LTi) and T
METHODS
METHODS
We performed flow cytometry of cerebellar and splenic tissue of MP4-immunized mice in the acute and chronic stage of the disease to analyze the presence of CD3
RESULTS
RESULTS
While we were able to detect LTi cells in the embryonic spleen and adult intestine, which served as positive controls, there was no evidence for the existence of such a population in acute or chronic EAE in neither of the two models. Yet, we detected CD3
CONCLUSION
CONCLUSIONS
The absence of LTi cells in the cerebellum suggests that other cells might take over the function as an initiator of lymphoid tissue formation in the CNS. Overall, the development of ectopic lymphoid organs is a complex process based on an interplay between several molecules and signals. Here, we propose some potential candidates, which might be involved in the formation of B cell aggregates in the CNS of MP4-immunized mice.
Identifiants
pubmed: 31138214
doi: 10.1186/s12974-019-1500-x
pii: 10.1186/s12974-019-1500-x
pmc: PMC6540524
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
111Subventions
Organisme : Deutsche Forschungsgemeinschaft
ID : KU2760/4-1
Références
Nat Med. 2000 Apr;6(4):435-42
pubmed: 10742151
Am J Surg Pathol. 2000 Jun;24(6):846-52
pubmed: 10843287
J Immunol. 2001 Jun 1;166(11):6593-601
pubmed: 11359812
Immunity. 2002 Jul;17(1):31-40
pubmed: 12150889
Nat Rev Immunol. 2003 Apr;3(4):292-303
pubmed: 12669020
Eur J Neurosci. 2003 Sep;18(5):1050-60
pubmed: 12956705
Genomics. 2004 Apr;83(4):727-34
pubmed: 15028294
Brain Pathol. 2004 Apr;14(2):164-74
pubmed: 15193029
Science. 2004 Jul 9;305(5681):248-51
pubmed: 15247480
J Exp Med. 2005 Jan 17;201(2):233-40
pubmed: 15657292
J Neurol Neurosurg Psychiatry. 2006 Feb;77(2):185-8
pubmed: 16421119
Nat Rev Immunol. 2006 Mar;6(3):205-17
pubmed: 16498451
Nat Immunol. 2006 Apr;7(4):344-53
pubmed: 16550197
J Neuroimmunol. 2006 Aug;177(1-2):99-111
pubmed: 16781782
Brain. 2007 Apr;130(Pt 4):1089-104
pubmed: 17438020
Immunity. 2007 May;26(5):643-54
pubmed: 17521585
J Neuroimmunol. 2007 Sep;189(1-2):31-40
pubmed: 17655940
Eur J Immunol. 2007 Nov;37(11):3240-5
pubmed: 17948268
Clin Immunol. 2008 Nov;129(2):256-67
pubmed: 18722816
J Immunol. 2009 Aug 15;183(4):2217-21
pubmed: 19635901
Immunity. 2011 Jan 28;34(1):122-34
pubmed: 21194981
Clin Immunol. 2011 Jul;140(1):54-62
pubmed: 21489887
Immunity. 2011 Dec 23;35(6):986-96
pubmed: 22177922
Mol Med. 2012 Sep 07;18:1018-28
pubmed: 22669475
Acta Neuropathol. 2012 Dec;124(6):861-73
pubmed: 22842876
Eur J Immunol. 2012 Sep;42(9):2255-62
pubmed: 22949324
Nat Rev Immunol. 2013 Feb;13(2):145-9
pubmed: 23348417
PLoS One. 2014 Apr 23;9(4):e94196
pubmed: 24759759
J Clin Invest. 2015 Jan;125(1):129-40
pubmed: 25415436
Clin Immunol. 2015 May;158(1):47-58
pubmed: 25796192
Immunity. 2015 Dec 15;43(6):1160-73
pubmed: 26682987
J Autoimmun. 2016 May;69:24-37
pubmed: 26922382
J Neuropathol Exp Neurol. 2016 Sep;75(9):877-88
pubmed: 27413074
Front Immunol. 2016 Oct 25;7:451
pubmed: 27826298
J Neuroinflammation. 2017 Jul 24;14(1):148
pubmed: 28738885
J Neuroinflammation. 2018 Aug 11;15(1):225
pubmed: 30098594
J Exp Med. 1996 Apr 1;183(4):1461-72
pubmed: 8666904
Immunity. 1997 Oct;7(4):493-504
pubmed: 9354470
J Immunol. 1998 Nov 1;161(9):4480-3
pubmed: 9794370