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Sodium chloride promotes pro-inflammatory macrophage polarization thereby aggravating CNS autoimmunity.
Teriflunomide treatment for multiple sclerosis modulates T cell mitochondrial respiration with affinity-dependent effects
Data demonstrate that high-affinity T cells preferentially use mitochondrial respiration, which is then inhibited by teriflunomide, and point to a mechanism of action where DHODH inhibition corrects metabolic disturbances in T cells, which primarily affects profoundly metabolically active high-Affinity T cell clones.
Signaling mechanisms inducing hypo-responsiveness of phagocytes during systemic inflammation.
The data indicate that the use of pharmacological JAK-STAT inhibitors may be promising targets for future therapeutic approaches to prevent complications associated with secondary hypo-responsiveness during SIRS.
Transcriptome Assessment Reveals a Dominant Role for TLR4 in the Activation of Human Monocytes by the Alarmin MRP8
The data confirm the primary importance of the TLR4/MRP8 axis in the activation of human monocytes, representing a novel and attractive target for modulation of the overwhelming innate immune response.
The farnesoid-X-receptor in myeloid cells controls CNS autoimmunity in an IL-10-dependent fashion
An important role of FXR is proposed in control of T cell-mediated autoimmunity by promoting anti-inflammatory macrophage responses in mice and in humans from healthy controls and MS patients.