about
Lethal host-versus-graft disease and hypereosinophilia in the absence of MHC I-T-cell interactions.Sex Differences in Plasmacytoid Dendritic Cell Levels of IRF5 Drive Higher IFN-α Production in Women.Interleukin 4-producing CD4 T cells arise from different precursors depending on the conditions of antigen exposure in vivo.Understanding the oestrogen action in experimental and clinical atherosclerosis.Bispecificity for myelin and neuronal self-antigens is a common feature of CD4 T cells in C57BL/6 mice.Selective immunosuppression.Impaired antigen presentation by murine I-Ad class II MHC molecules expressed in normal and HLA-DM-defective human B cell lines.Manipulation of the Th1/Th2 cell balance: an approach to treat human autoimmune diseases?Exogenous peptides compete for the presentation of endogenous antigens to major histocompatibility complex class II-restricted T cells.Selective immunosuppression by administration of major histocompatibility complex class II-binding peptides. II. Preventive inhibition of primary and secondary in vivo antibody responses.17Beta-estradiol promotes TLR4-triggered proinflammatory mediator production through direct estrogen receptor alpha signaling in macrophages in vivo.Endothelial estrogen receptor-alpha plays a crucial role in the atheroprotective action of 17beta-estradiol in low-density lipoprotein receptor-deficient mice.Protein kinase C-mediated calcium entry dependent upon dihydropyridine sensitive channels: a T cell receptor-coupled signaling pathway involved in IL-4 synthesis.Estrogen receptor α signaling in T lymphocytes is required for estradiol-mediated inhibition of Th1 and Th17 cell differentiation and protection against experimental autoimmune encephalomyelitis.Androgen signaling negatively controls group 2 innate lymphoid cells.Estrogen receptor alpha expression in both endothelium and hematopoietic cells is required for the accelerative effect of estradiol on reendothelialization.Role of inflammatory cytokines in the effect of estradiol on atheroma.The cGMP/protein kinase G pathway contributes to dihydropyridine-sensitive calcium response and cytokine production in TH2 lymphocytes.TLR7 escapes X chromosome inactivation in immune cells.Estrogens and inflammatory autoimmune diseases.Estradiol promotes functional responses in inflammatory and steady-state dendritic cells through differential requirement for activation function-1 of estrogen receptor α.X-Chromosome complement and estrogen receptor signaling independently contribute to the enhanced TLR7-mediated IFN-α production of plasmacytoid dendritic cells from women.The TLR-mediated response of plasmacytoid dendritic cells is positively regulated by estradiol in vivo through cell-intrinsic estrogen receptor α signaling.Endogenous estrogens, through estrogen receptor α, constrain autoimmune inflammation in female mice by limiting CD4+ T-cell homing into the CNS.MHC class II molecules bind indiscriminately self and non-self peptide homologs: effect on the immunogenicity of non-self peptides.Protein kinase C-dependent activation of CaV1.2 channels selectively controls human TH2-lymphocyte functions.Knocking down Cav1 calcium channels implicated in Th2 cell activation prevents experimental asthma.Estrogen Signaling in Bystander Foxp3 CD4 T Cells Suppresses Cognate Th17 Differentiation in and Protects from Central Nervous System AutoimmunityFemale predisposition to TLR7-driven autoimmunity: gene dosage and the escape from X chromosome inactivationA spontaneous hybridoma producing autoanti-idiotypic antibodies that recognize a V kappa-associated idiotope in mercury-induced autoimmunityMapping of a gene for the Mr 48,000 tubular basement membrane antigen in the ratDR alpha: E beta heterodimers in DRA transgenic mice hinder expression of E alpha: E beta molecules and are more efficient in antigen presentationThe mode of protein antigen administration determines preferential presentation of peptide-class II complexes by lymph node dendritic or B cellsB cells present antigen to CD4+ T cells, but fail to produce IL-12. Selective APC for Th2 cell development?Normal B cells fail to secrete interleukin-12Is pathogenic humoral autoimmunity a Th1 response?Regulation of the IL-12 receptor beta2 subunit by soluble antigen and IL-12 in vivoPolarization toward the T-helper(Th)1 type immune response is not required for rat experimental autoimmune myasthenia gravisBlockade of CD86 in BALB/c mice infected with Leishmania major does not prevent the expansion of low avidity T cellsCalcium channel blocker prevents T helper type 2 cell-mediated airway inflammation
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description
onderzoeker
@nl
researcher
@en
հետազոտող
@hy
name
Jean-Charles Guéry
@ast
Jean-Charles Guéry
@en
Jean-Charles Guéry
@es
Jean-Charles Guéry
@nl
type
label
Jean-Charles Guéry
@ast
Jean-Charles Guéry
@en
Jean-Charles Guéry
@es
Jean-Charles Guéry
@nl
altLabel
Jean-Charles GUERY
@en
prefLabel
Jean-Charles Guéry
@ast
Jean-Charles Guéry
@en
Jean-Charles Guéry
@es
Jean-Charles Guéry
@nl
P214
P1053
G-1452-2013
P106
P214
P2798
P31
P496
0000-0003-4499-3270
P7859
viaf-208832309