The role of CD30 in atopic disease

Bengtsson, Å.

doi:10.1034/j.1398-9995.2001.00137.x

Cited by 38 publications

(33 citation statements)

References 109 publications

(165 reference statements)

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“…In parallel, in a similar approach using a model of atopic conjunctivitis, treatment with an agonistic anti-4-1BB before or after sensitization abolished the development of allergic conjunctivitis [29]. For CD30, several studies have shown indirect evidence for a role in allergic diseases by correlating CD30 expression and sCD30 levels to severity and outcome of allergic asthma and atopic dermatitis [31][32][33]. By using CD30 −/− mice and mAbs directed against CD30 receptor or ligand, we could directly demonstrate a critical role of CD30 signalling in the development of asthma [16,17].…”

Section: Discussionmentioning

confidence: 94%

CD27 costimulation is not critical for the development of asthma and respiratory tolerance in a murine model

Behrendt

Hansen

2010

Immunology Letters

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Section: Discussionmentioning

confidence: 94%

CD27 costimulation is not critical for the development of asthma and respiratory tolerance in a murine model

Behrendt

Hansen

2010

Immunology Letters

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“…There are several lines of evidence showing that the CD30L-CD30 signaling is involved in Th2 cell responses and Th2-associated diseases (15)(16)(17)(18). Treating OVA-immunized WT mice with anti-CD153 mAb resulted in significantly reduced airway inflammation, serum IgE and Th2 cytokine levels.…”

Section: Discussionmentioning

confidence: 99%

“…CD30, the receptor for CD30L, and belonging to the TNFRSF, was reported to be expressed preferentially by activated or memory Th2 cells but not by resting B or T cells (12)(13)(14). CD30L/CD30 signaling was thought to be involved in Th2 cell responses and Th2-associated diseases (15)(16)(17)(18). However, a number of recent studies suggested that CD30L/CD30 signaling is also linked to Th1 cell responses and Th1-associated diseases (19 -22).…”

mentioning

confidence: 99%

A Novel Role of CD30L/CD30 Signaling by T-T Cell Interaction in Th1 Response against Mycobacterial Infection

Tang¹,

Yamada²,

Shibata³

et al. 2008

The Journal of Immunology

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A CD30 ligand (CD30L, CD153) is a type II membrane-associated glycoprotein belonging to the TNF family. To illustrate the potential role of CD30L in CD4+ Th1 cell responses, we investigated the fate of Ag-specific CD4+ T cells in CD30L-deficient (CD30L−/−) mice after Mycobacterium bovis bacillus Calmette-Guérin (BCG) infection. The number of bacteria was significantly higher in organs of CD30L−/− mice than in wild-type (WT) mice 4 wk postinfection. The numbers of purified protein derivative- or Ag85B-specific-IFN-γ-producing-CD4+ T cells in spleen, lung, or peritoneal exudate cells were significantly fewer in CD30L−/− mice than in WT mice. During the infection, CD30L was expressed mainly by CD44+CD3+CD4+ T cells but not by CD3+CD8+ T cells, B cells, dendritic cells, or macrophages. Costimulation with agonistic anti-CD30 mAb or coculturing with CD30L-transfected P815 cells restored IFN-γ production by CD4+ T cells from BCG-infected CD30L−/− mice. Coculturing with CD30L+/+CD4+ T cells from BCG-infected WT mice also restored the number of IFN-γ+CD30L−/−CD4+ T cells. When transferred into the CD30L+/+ mice, Ag-specific donor CD30L−/− CD4+ T cells capable of producing IFN-γ were restored to the compared level seen in CD30L+/+ CD4+ T cells on day 10 after BCG infection. When naive CD30L+/+ T cells were transferred into CD30L−/− mice, IFN-γ-producing-CD4+ Th1 cells of donor origin were normally generated following BCG infection, and IFN-γ-producing-CD30L−/−CD4+ Th1 cells of host origin were partly restored. These results suggest that CD30L/CD30 signaling executed by CD30+ T-CD30L+ T cell interaction partly play a critical role in augmentation of Th1 response capable of producing IFN-γ against BCG infection.

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“…These results suggested that CD30L/CD30 signaling is linked to Th1 cell responses and Th1-associated diseases. However, there are several observations that CD30L/CD30 signaling is involved in Th2 cell responses (39,40) and in naturally occurring Treg responses (23,24). Thus, CD30 signaling may not be linked to a commitment step for the differentiation of a specific Th cell subset.…”

Section: /2mentioning

confidence: 99%

CD30 Ligand/CD30 Plays a Critical Role in Th17 Differentiation in Mice

Sun

Yamada²,

Shibata³

et al. 2010

The Journal of Immunology

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A CD30 ligand (CD30L; CD153) and its receptor, CD30, is a membrane-associated glycoprotein belonging to the TNF superfamily and TNFR superfamily. These were expressed preferentially by activated CD4+T cells. In this paper, we show that CD44lowCD62hiCD4+ T cells from CD30L−/− or CD30−/− mice exhibited impaired differentiation into Th17 cells but an increased ability to produce IL-2 after in vitro culture under Th17-polarizing conditions. Neutralization with IL-2 by anti–IL-2 mAb partly restored the ability of Th17 differentiation in CD30L−/− or CD30−/− T cells. Stimulation via CD30L by immobilized anti-CD30L mAb suppressed IL-2 production by CD30−/−CD4+ T cells, indicating that the reverse signal to CD30L is responsible for downregulation of IL-2 production. In vivo Th17 differentiation of CD30L−/−CD4+CD45RBhigh T cells was also impaired after transfer into SCID mice, whereas CD30L+/+CD4+CD45RBhigh T cells normally differentiated into Th17 cells in CD30L−/−SCID mice. The results of these studies demonstrate that CD30L/CD30 signaling executed by the T-T cell interaction plays a critical role in Th17 cell differentiation, at least partly via downregulation of IL-2 production.

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The role of CD30 in atopic disease

Cited by 38 publications

References 109 publications

CD27 costimulation is not critical for the development of asthma and respiratory tolerance in a murine model

CD27 costimulation is not critical for the development of asthma and respiratory tolerance in a murine model

A Novel Role of CD30L/CD30 Signaling by T-T Cell Interaction in Th1 Response against Mycobacterial Infection

CD30 Ligand/CD30 Plays a Critical Role in Th17 Differentiation in Mice

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