The TNF Receptor Family Member CD30 Is Not Essential for Negative Selection

Deyoung, A.; Duramad, Omar; Winoto, Astar

doi:10.4049/jimmunol.165.11.6170

Cited by 47 publications

(25 citation statements)

References 32 publications

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“…CD30, another TNF receptor superfamily member originally suggested to be involved in negative selection [48] was later shown not to be involved in this process [49].…”

Section: Apoptosis In the Immune System Central Tolerance -Education mentioning

confidence: 99%

How apoptosis got the immune system in shape

Feig

Marynen

2007

Eur. J. Immunol.

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“…CD30, another TNF receptor superfamily member originally suggested to be involved in negative selection [48] was later shown not to be involved in this process [49].…”

Section: Apoptosis In the Immune System Central Tolerance -Education mentioning

confidence: 99%

How apoptosis got the immune system in shape

Feig

Marynen

2007

Eur. J. Immunol.

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“…CD30-deficient mice have been reported to have a defect in negative selection (10), and overexpression of CD30 on T cells results in augmented thymocyte depletion upon treatment with superantigen or antigenic peptide (11). However, a more recent study failed to confirm decreased negative selection in independently generated CD30-deficient mice (12), suggesting an alternative, as yet unidentified, role for CD30 in vivo.…”

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confidence: 99%

TCR-Independent CD30 Signaling Selectively Induces IL-13 Production Via a TNF Receptor-Associated Factor/p38 Mitogen-Activated Protein Kinase-Dependent Mechanism

Harlin

Podack

Boothby

et al. 2002

The Journal of Immunology

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Initiation of T lymphocyte responses to most Ags requires concurrent stimulation through the TCR and costimulatory receptors such as CD28. Following initial activation, secondary receptors are up-regulated that can costimulate T cells in concert with TCR engagement. One such receptor is the TNFR family member CD30. In this study, we report that unlike CD28, ligation of CD30 on normal effector T cells induces IL-13 production in the absence of concurrent TCR engagement. TCR-independent CD30-mediated IL-13 release correlated with activation of c-Jun N-terminal kinase, p38 mitogen-activated protein kinase (MAPK), and NF-κB, and was completely inhibited by the expression of a TNFR-associated factor 2 (TRAF2) dominant-negative transgene (TRAF2.DN-Tg), but not by that of an I-κBα dominant-negative transgene. In parallel, expression of the TRAF2.DN-Tg selectively prevented the induction of c-Jun N-terminal kinase and p38 MAPK, but not that of NF-κB. Furthermore, IL-13 production was reduced in a dose-dependent manner by the p38 MAPK inhibitor SB203580. Together, these results suggest that TCR-independent CD30-mediated production of IL-13 is triggered by association of CD30 with TRAF family members and subsequent activation of p38 MAPK. Inasmuch as IL-13 can promote airway inflammation and cancer progression, production of IL-13 in a TCR-independent manner has important pathological implications in vivo.

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“…Experiments using CD30-deficient mice have indicated that this molecule is involved in the deletion of autoreactive thymocytes (22,23), whereas a recent report denied this function (24). TNFR family members can transduce signals when surface molecules are appropriately cross-linked.…”

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confidence: 99%

Extremely Rapid and Intense Induction of Apoptosis in Human Eosinophils by Anti-CD30 Antibody Treatment In Vitro

Matsumoto

Terakawa

Miura

et al. 2004

The Journal of Immunology

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Apoptosis is an important cellular mechanism for controlling cell viability and proliferation. With respect to eosinophils, cytokines prolong their survival, whereas corticosteroids reduce their survival in vitro. CD30, a member of the TNFR family, is expressed on the surface of many cell types, including Hodgkin’s lymphoma cells. CD30 is capable of inducing apoptosis after Ab treatment in some cell lines. To determine whether this surface structure is involved in apoptosis of human eosinophils, we examined its expression and the effect of anti-CD30 Ab treatment on the viability of eosinophils. Purified human eosinophils expressed low, but consistently detectable, levels of CD30. Immobilized, but not soluble, forms of anti-CD30 Abs (HRS-4 and Ber-H8) or recombinant mouse CD30 ligand exhibited an extremely rapid and intense survival-reducing effect on the eosinophils in the presence of exogenous IL-5; this effect was both concentration and time dependent. Furthermore, high concentrations of IL-5 could not reverse the reduced survival rates. After treatment with anti-CD30 Ab, gel electrophoresis of DNA extracted from the eosinophils demonstrated changes consistent with apoptosis. The immobilized F(ab′)2 of the anti-CD30 Ab failed to induce eosinophil apoptosis. The addition of anti-CD18 Ab also completely abrogated the induction of eosinophil apoptosis. Further examination using specific signal transduction inhibitors suggested the involvement of p38, mitogen-activated protein kinase kinase 1/2, and specific tyrosine kinase, but not NF-κB, in the induction of CD30-mediated eosinophil apoptosis. These data demonstrate that CD30 can modify eosinophil survival by causing an extremely rapid and intense induction of apoptosis through a tightly regulated intracellular signaling pathway.

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The TNF Receptor Family Member CD30 Is Not Essential for Negative Selection

Cited by 47 publications

References 32 publications

How apoptosis got the immune system in shape

How apoptosis got the immune system in shape

TCR-Independent CD30 Signaling Selectively Induces IL-13 Production Via a TNF Receptor-Associated Factor/p38 Mitogen-Activated Protein Kinase-Dependent Mechanism

Extremely Rapid and Intense Induction of Apoptosis in Human Eosinophils by Anti-CD30 Antibody Treatment In Vitro

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