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Micro RNA-155 participates in re-activation of encephalitogenic T cells
Bojan Jevtić1, Gordana Timotijević2, Suzana Stanisavljević1
1Department of Immunology, Institute for Biological Research "SinišaStanković", University of Belgrade, Serbia.
Abstract:
MicroRNAs (miR) are small non-coding RNAs involved in the immune response regulation. miR-155 has been attributed a major pro-inflammatory role in the pathogenesis of multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE). Here, a role of miR-155 in re-activation of encephalitogenic CD4(+) T cells was investigated. Dark Agouti rats were immunized with myelin basic protein (MBP) emulsified in complete Freund's adjuvant. CD4(+) T cells were purified from draining lymph node cells (DLNC) obtained in the inductive phase and from spinal cord immune cells (SCIC) isolated at the peak of EAE. CD4(+) T cells obtained from SCIC (i.e., in vivo re-activated cells) had markedly higher expression of miR-155 in comparison to those purified from DLNC (not re-activated). Likewise, in vitro re-activation of DLNC with MBP led to increase in miR-155 expression. Further, DLNC and DLNC CD4(+) T cells were transfected with an inhibitor of miR-155 during in vitro re-activation. As a result, expression of important CD4(+) T cell effector cytokines IFN-γ and IL-17, but not of regulatory cytokines IL-10 and TGF-β, was reduced. These results imply that miR-155 supports re-activation of encephalitogenic CD4(+) T cells. Our results contribute to a view that miR-155 might be a valuable target in multiple sclerosis therapy.
Insights
MicroRNA-155 (miR-155) promotes the re-activation of T cells implicated in multiple sclerosis (MS). Inhibiting miR-155 reduced key inflammatory cytokines, suggesting it is a potential therapeutic target for MS.
Area of Science:
- Immunology
- Molecular Biology
- Neuroscience
Background:
- MicroRNAs (miRs) are small non-coding RNAs that regulate gene expression and play a role in immune responses.
- miR-155 is implicated in the pro-inflammatory pathogenesis of multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE).
- The specific role of miR-155 in the re-activation of encephalitogenic CD4(+) T cells in MS is not fully understood.
Purpose of the Study:
- To investigate the role of miR-155 in the re-activation of encephalitogenic CD4(+) T cells.
- To determine if miR-155 expression is altered during T cell re-activation in the context of EAE.
- To assess the impact of miR-155 inhibition on the expression of effector and regulatory cytokines in re-activated CD4(+) T cells.
Main Methods:
- Induction of EAE in Dark Agouti rats using myelin basic protein (MBP).
- Isolation and purification of CD4(+) T cells from draining lymph node cells (DLNC) and spinal cord immune cells (SCIC) at different disease phases.
- In vitro re-activation of DLNC with MBP and transfection with a miR-155 inhibitor.
- Quantification of miR-155 expression and key cytokine levels (IFN-γ, IL-17, IL-10, TGF-β) using RT-qPCR or similar techniques.
Main Results:
- CD4(+) T cells isolated from the spinal cord during peak EAE (in vivo re-activated) exhibited significantly higher miR-155 expression compared to those from draining lymph nodes (not re-activated).
- In vitro re-activation of DLNC with MBP led to an increase in miR-155 expression.
- Inhibition of miR-155 during in vitro re-activation reduced the expression of effector cytokines IFN-γ and IL-17, while levels of regulatory cytokines IL-10 and TGF-β remained unaffected.
Conclusions:
- miR-155 expression is upregulated during the re-activation of encephalitogenic CD4(+) T cells in EAE.
- miR-155 supports the re-activation of these T cells, likely by promoting the expression of key pro-inflammatory cytokines.
- These findings suggest that miR-155 could be a potential therapeutic target for managing multiple sclerosis by modulating T cell responses.
