Tertiary lymphoid organ development coincides with determinant spreading of the myelin-specific T cell response

Clicks: 114
ID: 114384
2012
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Steady

Ranked #351 of 438 articles by views in acta neuropathologica

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 438 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
While the role of T cells has been studied extensively in multiple sclerosis (MS), the pathogenic contribution of B cells has only recently attracted major attention, when it was shown that B cell aggregates can develop in the meninges of a subset of MS patients and were suggested to be correlates of late-stage and more aggressive disease in this patient population. However, whether these aggregates actually exist has subsequently been questioned and their functional significance has remained unclear. Here, we studied myelin basic protein (MBP)–proteolipid protein (PLP)-induced experimental autoimmune encephalomyelitis (EAE), which is one of the few animal models for MS that is dependent on B cells. We provide evidence that B cell aggregation is reflective of lymphoid neogenesis in the central nervous system (CNS) in MBP–PLP-elicited EAE. B cell aggregation was present already few days after disease onset. With disease progression CNS B cell aggregates increasingly displayed the phenotype of tertiary lymphoid organs (TLOs). Our results further imply that these TLOs were not merely epiphenomena of the disease, but functionally active, supporting intrathecal determinant spreading of the myelin-specific T cell response. Our data suggest that the CNS is not a passive “immune-privileged” target organ, but rather a compartment, in which highly active immune responses can perpetuate and amplify the autoimmune pathology and thereby autonomously contribute to disease progression.
Reference Key
kuerten2012actatertiary Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Stefanie Kuerten;Achim Schickel;Christian Kerkloh;Mascha S. Recks;Klaus Addicks;Nancy H. Ruddle;Paul V. Lehmann;Stefanie Kuerten;Achim Schickel;Christian Kerkloh;Mascha S. Recks;Klaus Addicks;Nancy H. Ruddle;Paul V. Lehmann;
Journal acta neuropathologica
Year 2012
DOI
doi:10.1007/s00401-012-1023-3
URL
https://link.springer.com/article/10.1007/s00401-012-1023-3
Keywords
pathology neurosciences

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.