Th2 responses induced by epicutaneous or inhalational protein exposure are differentially dependent on IL-4

Herrick, Christina A.; MacLeod, Heather; Glusac, Earl J.; Tigelaar, Robert E.; Bottomly, Kim

doi:10.1172/jci8624

Cited by 167 publications

(162 citation statements)

References 57 publications

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“…4). Neutrophilia in the BALF of EC-sensitized mice was reported by Herrick et al (29). A role for IL-17 in the recruitment of neutrophils to the airways and lungs of EC-sensitized mice was established by our demonstration that treatment of EC-sensitized mice with anti-IL-17A mAb before inhalation challenge resulted in a significantly decreased mRNA expression of CXCL2 and, more importantly, in a significant reduction in BALF neutrophilia (Fig.…”

Section: Discussionsupporting

confidence: 75%

Epicutaneous antigen exposure induces a Th17 response that drives airway inflammation after inhalation challenge

Oyoshi

Jin

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

184

163

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Section: Discussionsupporting

confidence: 75%

Epicutaneous antigen exposure induces a Th17 response that drives airway inflammation after inhalation challenge

Oyoshi

Jin

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

184

163

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“…The signals mediating APC-induced Th2 differentiation are less well understood. However, IL-4 and IL-6, as well as antigen dose, are thought to play a role [17,18]. Also, a pathway involving the Notch family of ligands, which seems to be cytokine independent, has been described.…”

Section: Discussionmentioning

confidence: 99%

Pertussis toxin-induced cytokine differentiation and clonal expansion of T cells is mediated predominantly via costimulation

Denkinger

Forsthuber

2007

Cellular Immunology

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Pertussis toxin (PTX) has potent immunologic adjuvant activity in vivo and concomitantly enhances both T helper type (Th) 1 and Th2 cytokine responses. The PTX-induced enhancement of Th1 and Th2 immunity is mediated via the activation of antigen presenting cells (APCs), but the underlying mechanism is not known.Here we asked whether the adjuvant activity of PTX on T cell immunity was mediated by cytokines and/or costimulatory signals.The results show that in vivo blockade of CD28-CD80/86 costimulation essentially abrogated PTXmediated enhancement of antigen-specific Th1 and Th2 responses. Blockade of CD40L-CD40 interactions was less efficient in inhibiting PTX-mediated enhancement of Th1 and Th2 responses. In contrast, the adjuvant activity of PTX was not mediated via cytokines, because neither Th1 nor Th2 responses were substantially impaired in mice deficient for IL-12, IFN-γ, IL-4, IL-5, or IL-6.Collectively, the data suggest that PTX mediates its adjuvant effects on T cell cytokine differentiation and clonal expansion via the modulation of costimulatory molecules on APCs. Understanding the costimulatory pathways targeted by PTX could lead to the design of novel adjuvants that selectively induce Th1 or Th2 immunity.

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“…Because the epicutaneous application of protein antigens can induce marked Th2 immune responses in mice (Herrick et al, 2000;Wang et al, 1996;Wang et al, 1999), we have tested the ability of this route of autoantigen delivery to impact on the development of EAE. We initially used transgenic mice with most T cells expressing a TCR specific for the N-terminal peptide (Ac1-11) of MBP (MBP TCR Tg mice) (Hardardottir et al, 1995;Lafaille, 2004).…”

Section: Suppressor T Cells Induced Via Epicutaneous Immunization Witmentioning

confidence: 99%

Control of experimental autoimmune encephalomyelitis by CD4+ suppressor T cells: Peripheral versus in situ immunoregulation

Bynoe

Bonorino

Viret

2007

Journal of Neuroimmunology

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The pathogenesis of experimental autoimmune encephalomyelitis (EAE) can be efficiently kept under control by specialized subsets of CD4+ T lymphocytes able to negatively regulate the function of T cells with encephalitogenic potential. A number of observations support a role for such suppressor T cells in controlling early phases of disease development at the level of peripheral lymphoid organs but there is also evidence suggesting immunoregulation within the central nervous system (CNS) microenvironment itself. This review evaluates the sites of regulation based on available data from distinct experimental models. We then discuss these aspects with reference to suppressor CD4+ T cells induced through the epicutaneous application of pure CNS antigens that confer long term protection against EAE. Finally, we give an overview of genes recently discovered to be important in regulation of the immune system that may also prove to be key players in the modulation of EAE and MS.

show abstract

Th2 responses induced by epicutaneous or inhalational protein exposure are differentially dependent on IL-4

Cited by 167 publications

References 57 publications

Epicutaneous antigen exposure induces a Th17 response that drives airway inflammation after inhalation challenge

Epicutaneous antigen exposure induces a Th17 response that drives airway inflammation after inhalation challenge

Pertussis toxin-induced cytokine differentiation and clonal expansion of T cells is mediated predominantly via costimulation

Control of experimental autoimmune encephalomyelitis by CD4+ suppressor T cells: Peripheral versus in situ immunoregulation

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