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Curcumin Inhibits Experimental Allergic Encephalomyelitis by Blocking IL-12 Signaling Through Janus Kinase-STAT Pathway in T Lymphocytes1
The findings highlight the fact that curcumin inhibits EAE by blocking IL-12 signaling in T cells and suggest its use in the treatment of MS and other Th1 cell-mediated inflammatory diseases.
Peroxisome proliferator-activated receptor-gamma agonists inhibit experimental allergic encephalomyelitis by blocking IL-12 production, IL-12 signaling and Th1 differentiation
The findings highlight the fact that PPARγ agonists regulate central nervous system inflammation and demyelination by inhibiting IL-12 production, IL- 12 signaling and Th1 differentiation in EAE.
TGF-beta inhibits IL-2-induced tyrosine phosphorylation and activation of Jak-1 and Stat 5 in T lymphocytes.
It is shown that treatment of activated T cells with TGF-beta inhibited IL-2-induced tyrosine phosphorylation and activation of Jak-1 and Stat 5 but not Jak-3 and Stat 3 and induced apoptotic cell death in T cells.
Differential regulation of CD4(+) T helper cell responses by curcumin in experimental autoimmune encephalomyelitis.
TGF-beta inhibits IL-12-induced activation of Jak-STAT pathway in T lymphocytes.
It is highlighted that TGF-beta inhibits IL-12-mediated responses by blocking IL- 12 signal transduction in T cells by inhibiting Jak kinases and tyrosine phosphorylation of STAT3 and STAT4 proteins.
Curcumin induces growth-arrest and apoptosis in association with the inhibition of constitutively active JAK-STAT pathway in T cell leukemia.
COX-2 Inhibitors Modulate IL-12 Signaling Through JAK-STAT Pathway Leading to Th1 Response in Experimental Allergic Encephalomyelitis
- G. Muthian, Himanshu P. Raikwar, J. Bright
- Biology, MedicineJournal of Clinical Immunology
- 1 January 2006
It is demonstrated that in vivo treatment with COX-2 inhibitors ameliorate EAE in association with the modulation of IL-12 signaling through JAK-STAT pathway leading to Th1 differentiation and suggest their use in the treatment of MS and other Th1 cell-mediated autoimmune diseases.
Expression of IL-12 in CNS and lymphoid organs of mice with experimental allergic encephalitis
Peroxisome proliferator‐activated receptor δ agonists inhibit T helper type 1 (Th1) and Th17 responses in experimental allergic encephalomyelitis
- Saravanan Kanakasabai, W. Chearwae, C. Walline, W. Iams, S. M. Adams, J. Bright
- Biology, MedicineImmunology
- 1 August 2010
It is shown that the PPARδ agonists GW501516 and L165041 are able to ameliorate MOGp35‐55‐induced EAE in C57BL/6 mice by blocking interferon (IFN)‐γ and interleukin (IL)‐17 production by Th1 and Th17 cells.