IL-11 induces surface marker expression and migration of T-lymphocytes

• Published in: The Journal of immunology (1950) Vol. 204; no. 1_Supplement; pp. 220 - 220.29
• Main Authors: Seyedsadr, Maryamsadat, Li, Jian, Markovic-Plese, Silva
• Format: Journal Article
• Language: English
• Published: 01.05.2020
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.204.Supp.220.29

Abstract Objective To study the phenotypic and migratory changes of PBMCs following IL-11 stimulation Background Multiple sclerosis (MS) is presumably an autoimmune disease in which immune cells mediate neuroinflammation and neurodegeneration in central nervous system. Cytokines play a significant role in orchestrating the inflammatory response during the disease. Our lab has previously shown that in untreated MS patients, IL-11 is upregulated in the CSF and serum in comparison to matched healthy controls (HCs). Previous study has shown that CD4+IL11+ cells are accumulated in the CSF and the brain MS lesions, suggesting that they play a role in the lesion formation. Methods 14 untreated RRMS patients and age-, sex- and race-matched HCs were enrolled in the study upon signing an Institutional Review Board consent forms. Results By using flow cytometry we characterized IL-11-secreting CD4+ lymphocytes and show that they have increased expression of CCR6, CCR4, ICAM-1, IL-11RA, GM-CSF, and IFNγ in comparison to CD4+IL-11− cells (p values<0.03). In vitro studies further showed that stimulation of PBMCs with recombinant human IL-11, upregulated the expression of CCR4 and CCR6 (p values<0.03, 1.2 and 1.4 fold changes) in CD4+ gated cells. In a trans-well system we observed that IL-11 can act as a chemoattractant for anti-CD3/CD28 mAb stimulated PBMCs and increase their migration (p value=0.04, migration index=1.2) in both patients and HCs. Conclusion We observed that IL-11 induces migratory phenotype in CD4+ lymphocytes in patients with RRMS, which can be explored as a therapeutic target in early RRMS.