Search

Your search keyword '"Croxford, J. Ludovic"' showing total 130 results
Start Over Author "Croxford, J. Ludovic"
130 results on '"Croxford, J. Ludovic"'

3. Supplementary Figure Legends from RAE1 Ligands for the NKG2D Receptor Are Regulated by STING-Dependent DNA Sensor Pathways in Lymphoma

Author

Lam, Adeline R., primary, Le Bert, Nina, primary, Ho, Samantha S.W., primary, Shen, Yu J., primary, Tang, Melissa L.F., primary, Xiong, Gordon M., primary, Croxford, J. Ludovic, primary, Koo, Christine X., primary, Ishii, Ken J., primary, Akira, Shizuo, primary, Raulet, David H., primary, and Gasser, Stephan, primary

Published
2023
Full Text
View/download PDF

4. Supplementary Figure 6 from RAE1 Ligands for the NKG2D Receptor Are Regulated by STING-Dependent DNA Sensor Pathways in Lymphoma

Author

Lam, Adeline R., primary, Le Bert, Nina, primary, Ho, Samantha S.W., primary, Shen, Yu J., primary, Tang, Melissa L.F., primary, Xiong, Gordon M., primary, Croxford, J. Ludovic, primary, Koo, Christine X., primary, Ishii, Ken J., primary, Akira, Shizuo, primary, Raulet, David H., primary, and Gasser, Stephan, primary

Published
2023
Full Text
View/download PDF

5. Supplementary Figure 3 from RAE1 Ligands for the NKG2D Receptor Are Regulated by STING-Dependent DNA Sensor Pathways in Lymphoma

Author

Lam, Adeline R., primary, Le Bert, Nina, primary, Ho, Samantha S.W., primary, Shen, Yu J., primary, Tang, Melissa L.F., primary, Xiong, Gordon M., primary, Croxford, J. Ludovic, primary, Koo, Christine X., primary, Ishii, Ken J., primary, Akira, Shizuo, primary, Raulet, David H., primary, and Gasser, Stephan, primary

Published
2023
Full Text
View/download PDF

6. Supplementary Figure 5 from RAE1 Ligands for the NKG2D Receptor Are Regulated by STING-Dependent DNA Sensor Pathways in Lymphoma

Author

Lam, Adeline R., primary, Le Bert, Nina, primary, Ho, Samantha S.W., primary, Shen, Yu J., primary, Tang, Melissa L.F., primary, Xiong, Gordon M., primary, Croxford, J. Ludovic, primary, Koo, Christine X., primary, Ishii, Ken J., primary, Akira, Shizuo, primary, Raulet, David H., primary, and Gasser, Stephan, primary

Published
2023
Full Text
View/download PDF

8. Supplementary Figure 2 from RAE1 Ligands for the NKG2D Receptor Are Regulated by STING-Dependent DNA Sensor Pathways in Lymphoma

Author

Lam, Adeline R., primary, Le Bert, Nina, primary, Ho, Samantha S.W., primary, Shen, Yu J., primary, Tang, Melissa L.F., primary, Xiong, Gordon M., primary, Croxford, J. Ludovic, primary, Koo, Christine X., primary, Ishii, Ken J., primary, Akira, Shizuo, primary, Raulet, David H., primary, and Gasser, Stephan, primary

Published
2023
Full Text
View/download PDF

9. Supplementary Figure 4 from RAE1 Ligands for the NKG2D Receptor Are Regulated by STING-Dependent DNA Sensor Pathways in Lymphoma

Author

Lam, Adeline R., primary, Le Bert, Nina, primary, Ho, Samantha S.W., primary, Shen, Yu J., primary, Tang, Melissa L.F., primary, Xiong, Gordon M., primary, Croxford, J. Ludovic, primary, Koo, Christine X., primary, Ishii, Ken J., primary, Akira, Shizuo, primary, Raulet, David H., primary, and Gasser, Stephan, primary

Published
2023
Full Text
View/download PDF

10. Supplementary Figure 7 from RAE1 Ligands for the NKG2D Receptor Are Regulated by STING-Dependent DNA Sensor Pathways in Lymphoma

Author

Lam, Adeline R., primary, Le Bert, Nina, primary, Ho, Samantha S.W., primary, Shen, Yu J., primary, Tang, Melissa L.F., primary, Xiong, Gordon M., primary, Croxford, J. Ludovic, primary, Koo, Christine X., primary, Ishii, Ken J., primary, Akira, Shizuo, primary, Raulet, David H., primary, and Gasser, Stephan, primary

Published
2023
Full Text
View/download PDF

11. Supplementary Figure 1 from RAE1 Ligands for the NKG2D Receptor Are Regulated by STING-Dependent DNA Sensor Pathways in Lymphoma

Author

Lam, Adeline R., primary, Le Bert, Nina, primary, Ho, Samantha S.W., primary, Shen, Yu J., primary, Tang, Melissa L.F., primary, Xiong, Gordon M., primary, Croxford, J. Ludovic, primary, Koo, Christine X., primary, Ishii, Ken J., primary, Akira, Shizuo, primary, Raulet, David H., primary, and Gasser, Stephan, primary

Published
2023
Full Text
View/download PDF

14. Direct suppression of CNS autoimmune inflammation via the cannabinoid receptor CB1 on neurons and CB2 on autoreactive T cells

Author

Maresz, Katarzyna, Pryce, Gareth, Ponomarev, Eugene D, Marsicano, Giovanni, Croxford, J Ludovic, Shriver, Leah P, Ledent, Catherine, Cheng, Xiaodong, Carrier, Erica J, Mann, Monica K, Giovannoni, Gavin, Pertwee, Roger G, Yamamura, Takashi, Buckley, Nancy E, Hillard, Cecilia J, Lutz, Beat, Baker, David, and Dittel, Bonnie N

Abstract

Author(s): Katarzyna Maresz [1, 11]; Gareth Pryce [2, 10, 11]; Eugene D Ponomarev [1]; Giovanni Marsicano [3]; J Ludovic Croxford [2, 4]; Leah P Shriver [1, 5]; Catherine Ledent [6]; [...]

Published
2007
Full Text
View/download PDF

16. Cannabinoids control spasticity and tremor in a multiple sclerosis model

Author

Baker, David, Pryce, Gareth, Croxford, J. Ludovic, Brown, Peter, Pertwee, Roger G., Huffman, John W., and Layward, Lorna

Subjects
Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Author(s): David Baker [1]; Gareth Pryce [1]; J. Ludovic Croxford [1]; Peter Brown [2]; Roger G. Pertwee [3]; John W. Huffman [4]; Lorna Layward Chronic relapsing experimental allergic encephalomyelitis (CREAE) [...]

Published
2000
Full Text
View/download PDF

26. RAE1 Ligands for the NKG2D Receptor Are Regulated by STING-Dependent DNA Sensor Pathways in Lymphoma

Author

Lam, Adeline R., primary, Le Bert, Nina, additional, Ho, Samantha S.W., additional, Shen, Yu J., additional, Tang, Melissa L.F., additional, Xiong, Gordon M., additional, Croxford, J. Ludovic, additional, Koo, Christine X., additional, Ishii, Ken J., additional, Akira, Shizuo, additional, Raulet, David H., additional, and Gasser, Stephan, additional

Published
2014
Full Text
View/download PDF

27. Cannabinoid-mediated neuroprotection, not immunosuppression, may be more relevant to multiple sclerosis.

Author

Croxford, J Ludovic, Pryce, Gareth, Jackson, Samuel J, Ledent, Catherine, Giovannoni, Gavin, Pertwee, Roger G, Yamamura, Takashi, Baker, David, Croxford, J Ludovic, Pryce, Gareth, Jackson, Samuel J, Ledent, Catherine, Giovannoni, Gavin, Pertwee, Roger G, Yamamura, Takashi, and Baker, David

Abstract

Cannabinoids may exhibit symptom control in multiple sclerosis (MS). We show here that cannabinoid receptor (CBR) agonists can also be immunosuppressive and neuroprotective in models of MS. Immunosuppression was associated with reduced: myelin-specific T cell responses; central nervous system infiltration and reduced clinical disease. This was found to be largely CB(1)R-dependent and only occurred at doses that induced significant cannabimimetic effects that would not be achieved clinically. Lower, non-immunosuppressive doses of cannabinoids however, slowed the accumulation of nerve loss and disability, despite failing to inhibit relapses. This further highlights the neuroprotective potential of cannabinoids to slow the progression of MS., Journal Article, Research Support, Non-U.S. Gov't, info:eu-repo/semantics/published

Published
2008

28. Direct suppression of CNS autoimmune inflammation via the cannabinoid receptor CB1 on neurons and CB2 on autoreactive T cells

Author

UCL, Maresz, Katarzyna, Pryce, Gareth, Ponomarev, Eugene D., Marsicano, Giovanni, Croxford, J. Ludovic, Shriver, Leah P., Ledent, Catherine, Cheng, Xiaodong, Carrier, Erica J., Mann, Monica K., Giovannoni, Gavin, Pertwee, Roger G., Yamamura, Takashi, Buckley, Nancy E., Hillard, Cecilia J., Lutz, Beat, Baker, David, Dittel, Bonnie N., UCL, Maresz, Katarzyna, Pryce, Gareth, Ponomarev, Eugene D., Marsicano, Giovanni, Croxford, J. Ludovic, Shriver, Leah P., Ledent, Catherine, Cheng, Xiaodong, Carrier, Erica J., Mann, Monica K., Giovannoni, Gavin, Pertwee, Roger G., Yamamura, Takashi, Buckley, Nancy E., Hillard, Cecilia J., Lutz, Beat, Baker, David, and Dittel, Bonnie N.

Abstract

The cannabinoid system is immunomodulatory and has been targeted as a treatment for the central nervous system (CNS) autoimmune disease multiple sclerosis. Using an animal model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE), we investigated the role of the CB1 and CB2 cannabinoid receptors in regulating CNS autoimmunity. We found that CB1 receptor expression by neurons, but not T cells, was required for cannabinoid-mediated EAE suppression. In contrast, CB2 receptor expression by encephalitogenic T cells was critical for controlling inflammation associated with EAE. CB2-deficient T cells in the CNS during EAE exhibited reduced levels of apoptosis, a higher rate of proliferation and increased production of inflammatory cytokines, resulting in severe clinical disease. Together, our results demonstrate that the cannabinoid system within the CNS plays a critical role in regulating autoimmune inflammation, with the CNS directly suppressing T-cell effector function via the CB2 receptor.

Published
2007

29. Cannabinoid-mediated immunosuppression in experimental allergic encephalomyelitis

Author

UCL - Autre, Baker, David, Croxford, J. Ludovic, Pryce, Gareth, Jackson, Samuel M., Ledent, Catherine, Marsicano, Giovanni, Lutz, Beat, Giovannoni, Gavin, Pertwee, Roger G., Yamamura, Takashi, 8th International Conference of Neuroimmunology, UCL - Autre, Baker, David, Croxford, J. Ludovic, Pryce, Gareth, Jackson, Samuel M., Ledent, Catherine, Marsicano, Giovanni, Lutz, Beat, Giovannoni, Gavin, Pertwee, Roger G., Yamamura, Takashi, and 8th International Conference of Neuroimmunology

Published
2006

33. Suppression of Experimental Autoimmune Encephalomyelitis by Ghrelin

Author

Theil, Michael-Mark, primary, Miyake, Sachiko, additional, Mizuno, Miho, additional, Tomi, Chiharu, additional, Croxford, J. Ludovic, additional, Hosoda, Hiroshi, additional, Theil, Julia, additional, von Hörsten, Stephan, additional, Yokote, Hiroaki, additional, Chiba, Asako, additional, Lin, Youwei, additional, Oki, Shinji, additional, Akamizu, Takashi, additional, Kangawa, Kenji, additional, and Yamamura, Takashi, additional

Published
2009
Full Text
View/download PDF

42. Mouse Models of Multiple Sclerosis.

Author

Walker, John M., Perl, Andras, Fuller, Kevin G., Olson, Julie K., Howard, Laurence M., Croxford, J. Ludovic, and Miller, Stephen D.

Abstract

Experimental autoimmune encephalomyelitis (EAE) and Theiler's murine encephalitis virus-induced demyelinating disease (TMEV-IDD) are two clinically relevant murine models of multiple sclerosis (MS). Like MS, both are characterized by mononuclear cell infiltrate into the central nervous system and demyelination. EAE is induced by either the administration of protein or peptide in adjuvant or by the adoptive transfer of encephalitogenic T-cell blasts into naïve recipients. The relative merits of each of these protocols are compared. Depending on the type of question asked, different mouse strains and peptides are used. Different disease courses are observed with different strains and different peptides in active EAE. These variations are addressed, and grading of mice in EAE is discussed. In addition to EAE induction, useful references for other disease indicators, such as delayed-type hypersensitivity, in vitro proliferation, and immunohistochemistry, are provided. TMEV-IDD is a useful model for understanding the potential viral etiology of MS. This chapter provides detailed information on the preparation of viral stocks and subsequent intracerebral infection of mice. In addition, virus plaque assay and disease assessment are discussed. Recombinant TMEV strains have been created for the study of molecular mimicry; these strains incorporate 30 various amino acid myelin epitopes within the leader region of TMEV. [ABSTRACT FROM AUTHOR]

Published
2004
Full Text
View/download PDF

45. Endocannabinoids control spasticity in a multiple sclerosis model

Author

Baker, David, primary, Pryce, Gareth, additional, Croxford, J. Ludovic, additional, Brown, Peter, additional, Pertwee, Roger G., additional, Makriyannis, Alexandros, additional, Khanolkar, Atmaram, additional, Layward, Lorna, additional, Fezza, Filomena, additional, Bisogno, Tiziana, additional, and Marzo, Vincenzo Di, additional

Published
2000
Full Text
View/download PDF

49. Development of Experimental Autoimmune Encephalomyelitis Critically Depends on CD 137 Ligand Signaling.

Author

Martínez Gómez, Julia M., Croxford, J. Ludovic, Kim Pin Yeo, Angeli, Véronique, Schwarz, Herbert, and Casser, Stephan

Subjects
*MULTIPLE sclerosis, *AUTOIMMUNE diseases, *CENTRAL nervous system, *ENCEPHALOMYELITIS, *MYELIN oligodendrocyte glycoprotein, *T cells, *CYTOKINES, *LEUCOCYTES
Abstract

Multiple sclerosis (MS) is a degenerative autoimmune disease of the CNS. Experimental autoimmune encephalomyelitis (EAE) is a commonly used murine model for MS. Here we report that CD137 ligand (CD137L, 4-1BB ligand, TNFS9), a member of the TNF super-family, is critical for the development of EAE. EAE symptoms were significantly ameliorated in CD137L-/- mice. In the absence of CD137L, myelin oligodendrocyte glycoprotein (MOG)-specific T-cells secreted lower levels of Thl/Th17 cell-associated cytokines. MOG-specific T-cells also trafficked less efficiently to the CNS in CD 137L-/- mice, possibly as a consequence of reduced expression of vascular cell adhesion molecule-1 (VCAM-1), which regulates leukocyte extravasation. Thus, CD137L regulates many functions of MOG-specific T-cells that contribute to EAE and may represent a novel therapeutic target for the treatment of MS. [ABSTRACT FROM AUTHOR]

Published
2012
Full Text
View/download PDF

50. CD137 ligand activated microglia induces oligodendrocyte apoptosis via reactive oxygen species.

Author

Yee Andy Yeo, Mart�nez G�mez, Julia M., Croxford, J. Ludovic, Gasser, Stephan, Eng-Ang Ling, and Schwarz, Herbert

Subjects
TUMOR necrosis factors, LIGANDS (Biochemistry), APOPTOSIS, ENCEPHALOMYELITIS, CENTRAL nervous system diseases
Abstract

CD137 (4-1BB, TNFRSF9), a member of the tumor necrosis factor (TNF) receptor family, is a potent T cell co-stimulatory molecule. CD137 ligand (CD137L) is expressed by antigen presenting cells (APC) as a transmembrane protein and transmits activating signals into APC. In this study we investigated the effects of CD137L signaling in microglia, the resident APC in the central nervous system. In vitro, the murine microglia cell lines BV-2 and N9, as well as primary murine microglia responded with activation as evidenced by adherence and secretion of proinflammatory cytokines, MMP-9, and soluble intercellular adhesion molecule (ICAM). CD137L signaling is also important for microglia activation in vivo, since CD137L-deficient mice exhibited profoundly less microglia activation during experimental autoimmune encephalomyelitis (EAE) which is a well-established murine model for neuroinflammation and human multiple sclerosis (MS). Also CD137 is expressed in the CNS of mice during EAE. Activated microglia has been reported to mediate the destruction of axonal myelin sheaths and cause the death of oligodendrocytes, the main pathogenic mechanisms in EAE and MS. Corresponding to the lower microglia activation there were also fewer apoptotic oligodendrocytes in the CNS of CD137L-deficient mice. In vitro co-culture confirmed that CD137L-activated microglia induces apoptosis in oligodendrocytes, and identified reactive oxygen species as the mechanism of apoptosis induction. These data demonstrate activating effects of CD137L signaling to microglia, and show for the first time that the CD137 receptor/ligand system may be a mediator of neuroinflammatory and neurodegenerative disease, by activating microglia which in turn kill oligodendrocytes. [ABSTRACT FROM AUTHOR]

Published
2012
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results