Reduced annexin A1 expression associates with disease severity and inflammation in multiple sclerosis patients

Alessandra Colamatteo, Elisa Maggioli, Rodrigo Azevedo Loiola, Madeeha Hamid Sheikh, Gaetano Calì, Dario Bruzzese, Giorgia Teresa Maniscalco, Diego Centonze, Fabio Buttari, Roberta Lanzillo, Francesco Perna, Bruno Zuccarelli, Maria Mottola, Silvana Cassano, Mario Galgani, Egle Solito, Veronica De Rosa

Research output: Contribution to journalArticlepeer-review


Chronic neuroinflammation is a key pathological hallmark of multiple sclerosis (MS) that suggests that resolution of inflammation by specialized proresolving molecules is dysregulated in the disease. Annexin A1 (ANXA1) is a protein induced by glucocorticoids that facilitates resolution of inflammation through several mechanisms that include an inhibition of leukocyte recruitment and activation. In this study, we investigated the ability of ANXA1 to influence T cell effector function in relapsing/remitting MS (RRMS), an autoimmune disease sustained by proinflammatory Th1/Th17 cells. Circulating expression levels of ANXA1 in naive-to-treatment RRMS subjects inversely correlated with disease score and progression. At the cellular level, there was an impaired ANXA1 production by CD4+CD252 conventional T and CD4+RORgt+ T (Th17) cells from RRMS subjects that associated with an increased migratory capacity in an in vitro model of blood brain barrier. Mechanistically, ANXA1 impaired monocyte maturation secondarily to STAT3 hyperactivation and potently reduced T cell activation, proliferation, and glycolysis. Together, these findings identify impaired disease resolution pathways in RRMS caused by dysregulated ANXA1 expression that could represent new potential therapeutic targets in RRMS.

Original languageEnglish
Pages (from-to)1753-1765
Number of pages13
JournalJournal of Immunology
Issue number7
Publication statusPublished - Oct 1 2019

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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