The intensity of neutrophil infiltration controls the number of antigen-primed CD8 T cells recruited into cutaneous antigen challenge sites.
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Neutrophil trails guide influenza-specific CD8⁺ T cells in the airways.Novel concept of iSALT (inducible skin-associated lymphoid tissue) in the elicitation of allergic contact dermatitisHapten-induced contact hypersensitivity, autoimmune reactions, and tumor regression: plausibility of mediating antitumor immunityCutting edge: NLRP12 controls dendritic and myeloid cell migration to affect contact hypersensitivityCD8 T cells producing IL-17 and IFN-gamma initiate the innate immune response required for responses to antigen skin challenge.The role of neutrophils and G-CSF in DNFB-induced contact hypersensitivity in mice.Restraint stress fails to modulate cutaneous hypersensitivity responses in mice lacking the adenosine A1 receptor.Neutrophils are required for both the sensitization and elicitation phase of contact hypersensitivityIL-17 and IFN-gamma mediate the elicitation of contact hypersensitivity responses by different mechanisms and both are required for optimal responses.CD8+ IL-17-producing T cells are important in effector functions for the elicitation of contact hypersensitivity responses.Hapten application to the skin induces an inflammatory program directing hapten-primed effector CD8 T cell interaction with hapten-presenting endothelial cellsThe NF-κB regulator Bcl-3 modulates inflammation during contact hypersensitivity reactions in radioresistant cells.IL-1 receptor signaling is required at multiple stages of sensitization and elicitation of the contact hypersensitivity responseONZIN deficiency attenuates contact hypersensitivity responses in miceDisruption of the complement anaphylatoxin receptor C5L2 exacerbates inflammation in allergic contact dermatitisNeutrophil expression of Fas ligand and perforin directs effector CD8 T cell infiltration into antigen-challenged skin.Effects of the tumor microenvironment on the efficacy of tumor immunotherapy.Neutrophils are dispensable in the modulation of T cell immunity against cutaneous HSV-1 infection.Effector and regulatory mechanisms in allergic contact dermatitis.Immunological mechanisms of contact hypersensitivity in mice.Inflammatory and immune mechanisms in contact hypersensitivity (CHS) in rats.Intravital 2-photon imaging, leukocyte trafficking, and the beating heart.New concepts in cutaneous allergy.Contribution of CD4(+ )and CD8(+) T-cells in contact hypersensitivity and allergic contact dermatitis.Novel role of regulatory T cells in limiting early neutrophil responses in skin.Decorin potentiates interferon-γ activity in a model of allergic inflammation.The role for decorin in delayed-type hypersensitivityEpidermal NLRP10 contributes to contact hypersensitivity responses in mice.Attenuation of acute lung inflammation induced by cigarette smoke in CXCR3 knockout mice.Regulatory T cells can prevent memory CD8+ T-cell-mediated rejection following polymorphonuclear cell depletion.Elevated epidermal ornithine decarboxylase activity suppresses contact hypersensitivity.Aquaporin-9-expressing neutrophils are required for the establishment of contact hypersensitivity.[Immunology of contact allergy].Percutaneous toxicity of dinitrochlorobenzene (DNCB) in rats.Local and systemic effects of co-stimulatory blockade using cytotoxic T lymphocyte antigen-4-immunoglobulin in dinitrofluorobenzene- and oxazolone-induced contact hypersensitivity in mice.The effects of bovine colostrum supplementation on in vivo immunity following prolonged exercise: a randomised controlled trial.In Vivo Expansion of Endogenous Regulatory T Cell Populations Induces Long-Term Suppression of Contact Hypersensitivity.Serum CXCL1 concentrations are elevated in type 1 diabetes mellitus, possibly reflecting activity of anti-islet autoimmune activity.Leukotriene B₄-leukotriene B₄ receptor axis promotes oxazolone-induced contact dermatitis by directing skin homing of neutrophils and CD8⁺ T cells.Innate immunity and effector and regulatory mechanisms involved in allergic contact dermatitis.
P2860
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P2860
The intensity of neutrophil infiltration controls the number of antigen-primed CD8 T cells recruited into cutaneous antigen challenge sites.
description
2004 nî lūn-bûn
@nan
2004年の論文
@ja
2004年学术文章
@wuu
2004年学术文章
@zh-cn
2004年学术文章
@zh-hans
2004年学术文章
@zh-my
2004年学术文章
@zh-sg
2004年學術文章
@yue
2004年學術文章
@zh
2004年學術文章
@zh-hant
name
The intensity of neutrophil in ...... neous antigen challenge sites.
@en
The intensity of neutrophil in ...... neous antigen challenge sites.
@nl
type
label
The intensity of neutrophil in ...... neous antigen challenge sites.
@en
The intensity of neutrophil in ...... neous antigen challenge sites.
@nl
prefLabel
The intensity of neutrophil in ...... neous antigen challenge sites.
@en
The intensity of neutrophil in ...... neous antigen challenge sites.
@nl
P2093
P2860
P356
P1476
The intensity of neutrophil in ...... neous antigen challenge sites.
@en
P2093
Anton V Gorbachev
Danielle D Kish
Robert L Fairchild
Tara Engeman
P2860
P304
P356
10.1189/JLB.0304193
P577
2004-08-24T00:00:00Z