about
Proteomic and metabolomic analyses of mitochondrial complex I-deficient mouse model generated by spontaneous B2 short interspersed nuclear element (SINE) insertion into NADH dehydrogenase (ubiquinone) Fe-S protein 4 (Ndufs4) geneBreakdown in repression of IFN-γ mRNA leads to accumulation of self-reactive effector CD8+ T cells.The dominant role of CD8+ dendritic cells in cross-presentation is not dictated by antigen capture.CD8+ T cells from a novel T cell receptor transgenic mouse induce liver-stage immunity that can be boosted by blood-stage infection in rodent malaria.Cross-presentation, dendritic cell subsets, and the generation of immunity to cellular antigens.Putative IKDCs are functionally and developmentally similar to natural killer cells, but not to dendritic cellsPeripheral deletion of autoreactive CD8 T cells by cross presentation of self-antigen occurs by a Bcl-2-inhibitable pathway mediated by BimSOCS1: a potent and multifaceted regulator of cytokines and cell-mediated inflammation.Loss of Bim increases T cell production and function in interleukin 7 receptor-deficient miceSOCS-1 regulates IL-15-driven homeostatic proliferation of antigen-naive CD8 T cells, limiting their autoimmune potential.Blood-stage Plasmodium infection induces CD8+ T lymphocytes to parasite-expressed antigens, largely regulated by CD8alpha+ dendritic cells.The dendritic cell subtype-restricted C-type lectin Clec9A is a target for vaccine enhancementTissue destruction caused by cytotoxic T lymphocytes induces deletional tolerance.Transience of MHC Class I-restricted antigen presentation after influenza A virus infection.The molecular signature of CD8+ T cells undergoing deletional toleranceTargeting Antigen to Clec9A Primes Follicular Th Cell Memory Responses Capable of Robust Recall.Mouse CD8alpha+ DCs and human BDCA3+ DCs are major producers of IFN-lambda in response to poly IC.Cutting edge: priming of CD8 T cell immunity to herpes simplex virus type 1 requires cognate TLR3 expression in vivo.Development of a Novel CD4+ TCR Transgenic Line That Reveals a Dominant Role for CD8+ Dendritic Cells and CD40 Signaling in the Generation of Helper and CTL Responses to Blood-Stage Malaria.Blood-stage Plasmodium berghei infection leads to short-lived parasite-associated antigen presentation by dendritic cells.SOCS1 negatively regulates the production of Foxp3+ CD4+ T cells in the thymus.Blood-stage Plasmodium berghei infection generates a potent, specific CD8+ T-cell response despite residence largely in cells lacking MHC I processing machinery.IFN Regulatory Factor 3 Balances Th1 and T Follicular Helper Immunity during Nonlethal Blood-Stage Plasmodium Infection.Equivalent stimulation of naive and memory CD8 T cells by DNA vaccination: a dendritic cell-dependent process.Targeting antigen to mouse dendritic cells via Clec9A induces potent CD4 T cell responses biased toward a follicular helper phenotype.Aire regulates the transfer of antigen from mTECs to dendritic cells for induction of thymic tolerance.Kidney protection against autoreactive CD8(+) T cells distinct from immunoprivilege and sequestration.Cutting Edge: Enhanced IL-2 Signaling Can Convert Self-Specific T Cell Response from Tolerance to AutoimmunityIdentification of a MHC I-restricted epitope of DsRed in C57BL/6 miceGeneric construction of single component particles that elicit humoural and cellular immune responses without the need for adjuvantsSuppressor of Cytokine Signaling-1 Has IFN- -Independent Actions in T Cell HomeostasisCutting Edge: Precursor Frequency Affects the Helper Dependence of Cytotoxic T CellsCell-Associated Ovalbumin Is Cross-Presented Much More Efficiently than Soluble Ovalbumin In VivoA Bone Marrow-Derived APC in the Gut-Associated Lymphoid Tissue Captures Oral Antigens and Presents Them to Both CD4+ and CD8+ T CellsSuppressor of Cytokine Signaling-1 Regulates Signaling in Response to Interleukin-2 and Other γc-dependent Cytokines in Peripheral T CellsThymic shared antigen-2: a novel cell surface marker associated with T cell differentiation and activationCutting edge: TLR ligands are not sufficient to break cross-tolerance to self-antigens
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description
onderzoeker
@nl
researcher
@en
հետազոտող
@hy
name
Gayle M Davey
@ast
Gayle M Davey
@en
Gayle M Davey
@es
Gayle M Davey
@nl
type
label
Gayle M Davey
@ast
Gayle M Davey
@en
Gayle M Davey
@es
Gayle M Davey
@nl
prefLabel
Gayle M Davey
@ast
Gayle M Davey
@en
Gayle M Davey
@es
Gayle M Davey
@nl
P214
P244
P106
P214
P244
no2015054396
P31
P496
0000-0002-9514-6023
P734
P7859
lccn-no2015054396