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24 results on '"Gruber, Ross C."'

7. Establishing a Role for the Bruton’s Tyrosine Kinase Inhibitor Tolebrutinib in Modulating Neuroinflammation and Disease Progression in MS (1974)

Author

Gruber, Ross C., primary, Dufault, Michael R., additional, Chretien, Nathalie, additional, Proto, Jonathan D., additional, Zhang, Mindy, additional, Havari, Evis, additional, Turner, Timothy, additional, Chomyk, Anthony, additional, Christie, Emilie, additional, Trapp, Bruce D., additional, and Ofengeim, Dimitry, additional

Published
2021
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8. Central Effects of BTK Inhibition in Neuroinflammation (808)

Author

Gruber, Ross C., primary, Chretien, Nathalie, additional, Dufault, Michael R., additional, Proto, Jonathan, additional, Zhang, Mindy, additional, LaMorte, Michael, additional, Havari, Evis, additional, Samad, Tarek A., additional, Turner, Timothy, additional, Chomyk, Anthony, additional, Christie, Emilie, additional, Trapp, Bruce D., additional, and Ofengeim, Dimitry, additional

Published
2020
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11. Autophagy Is a Tolerance-Avoidance Mechanism that Modulates TCR-Mediated Signaling and Cell Metabolism to Prevent Induction of T Cell Anergy

Author

Cancer, CMM Groep Coffer, Infection & Immunity, Immuno/reuma onderzoek 5 (Vastert2), Child Health, CMM, Onderzoek, CMM Sectie Stem Cells, Regenerative Medicine and Stem Cells, Mocholi, Enric, Dowling, Samuel D., Botbol, Yair, Gruber, Ross C., Ray, Alex K., Vastert, Sebastiaan, Shafit-Zagardo, Bridget, Coffer, Paul J., Macian, Fernando, Cancer, CMM Groep Coffer, Infection & Immunity, Immuno/reuma onderzoek 5 (Vastert2), Child Health, CMM, Onderzoek, CMM Sectie Stem Cells, Regenerative Medicine and Stem Cells, Mocholi, Enric, Dowling, Samuel D., Botbol, Yair, Gruber, Ross C., Ray, Alex K., Vastert, Sebastiaan, Shafit-Zagardo, Bridget, Coffer, Paul J., and Macian, Fernando

Published
2018

14. Targeted GAS6 Delivery to the CNS Protects Axons from Damage during Experimental Autoimmune Encephalomyelitis

Author

National Institutes of Health (US), National Multiple Sclerosis Society (US), Gruber, Ross C., Ray, Alex K., Johndrow, Christopher T., Guzik, Hillary M., Burek, Dominika, García de Frutos, Pablo, Shaft-Zagardo, Bridget, National Institutes of Health (US), National Multiple Sclerosis Society (US), Gruber, Ross C., Ray, Alex K., Johndrow, Christopher T., Guzik, Hillary M., Burek, Dominika, García de Frutos, Pablo, and Shaft-Zagardo, Bridget

Abstract

Growth arrest-specific protein 6 (GAS6) is a soluble agonist of the TYRO3, AXL, MERTK (TAM) family of receptor tyrosine kinases identified to have anti-inflammatory, neuroprotective, and promyelinating properties. During experimental autoimmune encephalomyelitis (EAE), wild-type (WT) mice demonstrate a significant induction of Gas6, Axl, and Mertk but not Pros1 or Tyro3 mRNA. We tested the hypothesis that intracerebroventricular delivery of GAS6 directly into the CNS of WT mice during myelin oligodendrocyte glycoprotein (MOG)-induced EAE would improve the clinical course of disease relative to artificial CSF (ACSF)-treated mice. GAS6 did not delay disease onset, but significantly reduced the clinical scores during peak and chronic EAE. Mice receiving GAS6 for 28 d had preserved SMI31(+) neurofilament immunoreactivity, significantly fewer SMI32(+) axonal swellings and spheroids and less demyelination relative to ACSF-treated mice. Alternate-day subcutaneous IFNß injection did not enhance GAS6 treatment effectiveness. Gas6(-/-) mice sensitized with MOG35-55 peptide exhibit higher clinical scores during late peak to early chronic disease, with significantly increased SMI32(+) axonal swellings and Iba1(+) microglia/macrophages, enhanced expression of several proinflammatory mRNA molecules, and decreased expression of early oligodendrocyte maturation markers relative to WT mouse spinal cords with scores for 8 consecutive days. During acute EAE, flow cytometry showed significantly more macrophages but not T-cell infiltrates in Gas6(-/-) spinal cords than WT spinal cords. Our data are consistent with GAS6 being protective during EAE by dampening the inflammatory response, thereby preserving axonal integrity and myelination.

Published
2014

24. Regulation of avoidant behaviors and pain by the anti-inflammatory tyrosine phosphatase SHP-1.

Author

Hudson, Chad A., Christophi, George P., Cao, Ling, Gruber, Ross C., and Massa, Paul T.

Abstract

The protein tyrosine phosphatase SHP-1 is a critical regulator of cytokine signaling and inflammation. Mice homozygous for a null allele at the SHP-1 locus have a phenotype of severe inflammation and are hyper-responsive to the TLR4 ligand LPS. TLR4 stimulation in the CNS has been linked to both neuropathic pain and sickness behaviors. To determine if reduction in SHP-1 expression affects LPS-induced behaviors, responses of heterozygous SHP-1-deficient (me/+) and wild-type (+/+) mice to LPS were measured. Chronic (4-week) treatment with LPS induced avoidant behaviors indicative of fear/anxiety in me/+, but not +/+, mice. These behaviors were correlated with a LPS-induced type 2 cytokine, cytokine receptor, and immune effector arginase profile in the brains of me/+ mice not found in +/+ mice. Me/+ mice also had a constitutively greater level of TLR4 in the CNS than +/+ mice. Additionally, me/+ mice displayed constitutively increased thermal sensitivity compared to +/+ mice, measured by the tail-flick test. Moreover, me/+ glial cultures were more responsive to LPS than +/+ glia. Therefore, the reduced expression of SHP-1 in me/+ imparts haploinsufficiency with respect to the control of CNS TLR4 and pain signaling. Furthermore, type 2 cytokines become prevalent during chronic TLR4 hyperstimulation in the CNS and are associated positively with behaviors that are usually linked to type 1 pro-inflammatory cytokines. These findings question the notion that type 2 immunity is solely anti-inflammatory in the CNS and indicate that type 2 immunity induces/potentiates CNS inflammatory processes. [ABSTRACT FROM PUBLISHER]

Published
2007
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