In vivo CD30 expression in human diseases with predominant activation of Th2-like T cells

D’Elios, M M; Romagnani, Paola; Scaletti, Cristina; Annunziato, Francesco; Manghetti, M.; Mavilia, Carmelo; Parronchi, Paola; Pupilli, Cinzia; Pizzolo, Giovanni; Maggi, Enrico; Prete, G.; Romagnani, Sergio

doi:10.1002/jlb.61.5.539

Cited by 97 publications

(78 citation statements)

References 21 publications

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“…34 Increased serum levels of soluble CD30 have been correlated with Th2 cell activation and seen in chronic GVHD patients. 35 In multiple sclerosis, high levels of soluble CD30 are indicative of remission, presumably due to the down-regulation of the Th1 cell activation that leads to disease pathology. 36 Conceivably, polymorphisms in either 4-1BB or CD30 might influence the relative predominance of the Th1 vs Th2 subsets during development of GVHD.…”

Section: Discussionmentioning

confidence: 99%

Genetic factors influencing the development of chronic graft-versus-host disease in a murine model

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Dobkins

Harper

et al. 2000

Bone Marrow Transplant

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Summary:Graft-versus-host disease (GVHD) is a major complication of bone marrow transplantation that can occur in either acute or chronic forms. Much of the long-term pathology seen in chronic GVHD is a result of autoantibody production. In the DBA/2 → B6D2F1 murine model of chronic GVHD, anti-ssDNA autoantibodies can be detected by 14 days post cell transfer. These autoantibodies are not observed in B6D2F1 recipients of cells from C57BL/6 or B10.D2 donors, which develop acute rather than chronic GVHD. Therefore, in this model, donor genetic factors predispose to the development of chronic GVHD in recipients. We performed a genetic analysis aimed at mapping donor loci that influence the magnitude of early autoantibody production in B6D2F1 recipients of cells from DBA/2 donor mice. Linkage analysis suggested an influence of two loci: a locus on chromosome 11 linked to D11Mit278 and a locus on chromosome 4 linked to D4Mit226. The locus on chromosome 11 also appeared to influence the development of renal pathology associated with chronic GVHD. Bone Marrow Transplantation (2000) 26, 931-938.

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Section: Discussionmentioning

confidence: 99%

Genetic factors influencing the development of chronic graft-versus-host disease in a murine model

Slayback

Dobkins

Harper

et al. 2000

Bone Marrow Transplant

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“…The truncated and soluble form of CD30 is preferentially expressed and released by human T-cell clones with a Th2!fh0 phenotype in vitro (25). High serum levels of sCD30 have been prevalently found in Th2-dominated disorders, however they havealso been found in subjects with rheumatoid arthritis, a disease ascribed to Thl-induced mechanisms (19,26,31).…”

Section: Ifn-yand Il-4/il-5 Would Theoretically Represent the Best Tomentioning

confidence: 99%

“…In particular, the lymphocyte activation gene-3 (CD223) molecule has been shown to be expressed on, and released by, activated IFN-yproducing Thl cells (24), whereas the CD30 molecule has been shown to be expressed on, and released by, activated IL-4 producing CD4+ Th2 cells (25)(26). The determination of these soluble factors could provide insight into immune responses to vaccines in general, and particularly help clarify differences in the mechanisms of pertussis vaccines, which can induce both Th I and mixed Thlffh2 responses (3,(6)(7)(9)(10).…”

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confidence: 99%

Soluble CD30 and Lymphocyte Activation Gene-3 (CD223), as Potential Serological Markers of T Helper-Type Cytokine Response Induced by Acellular Pertussis Vaccine

Palazzo

Spensieri

et al. 2006

Int J Immunopathol Pharmacol

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T cell responses are involved in vaccine-induced immunity to pertussis but no easy-to-monitor, serological markers are available to assess these responses. The lymphocyte activation gene-3 (CD223) molecule is present on, and released by, activated T helper (Th) 1 cells, whereas CD30 molecules have been associated with Th2 immune responses. Starting from the recent knowledge of the cytokine profile induced by pertussis vaccination, we examined the levels of soluble (s)CD223 and sCD30 proteins in child recipients of acellular pertussis (aP) and diphtheria-tetanus (DT) vaccines and in children receiving DT vaccine only, as control. The correlation of the two proteins with specific antibody and T cell responses was assessed. The main findings are: i) sCD223 and sCD30 levels are inversely related, suggesting that the two markers are the expression of different and counter-regulated T-cell responses; ii) sCD30 level correlated with induction of T cell proliferation to pertussis vaccine antigens and antibody response to pertussis toxin. Overall, sCD30 and sCD223 levels seem to be promising candidate markers to assess the induction of Th-type responses in vaccine recipients.The mechanisms underlying induction of immune protection from Bordetella pertussis infection are not completely understood (I). Data from experimental infections and, in part, clinical studies suggest that natural immunity as well as T and B memory cell compartments are involved, but the differential contribution of each of these components in the protection induced by vaccination or disease-free natural exposure to B. pertussis or the disease itself remains largely undetermined (1-10). A correlation between high titers of antibodies against some B. pertussis antigens and protection of household contacts ofpertussis cases has been found (11-13), nevertheless, no direct correlation between serum antibody levels and protection from pertussis was found in several clinical trials with extended, carefully investigated, follow-up periods (14)(15)(16)(17)(18).Since the discovery of T helper (Th)l and Th2 lymphocyte subsets and their role in the regulation of immune response, studies have been intensely focused on the possibility of discriminating the prevalent expansion of CD4 lymphocytes with Th I or Th2 profile, in consideration to the differential role of each subset for vaccine efficacy. Thl .or Th2 are mainly discriminated through the pattern of their secreted cytokines, in that Thl subsets secrete interferon gamma (IFN-y) but not IL-4, while Th2 subsets secrete IL-4, IL-5, IL-6, IL-1O and IL-13 but not IFN-y However, a mixed pattern of cytokines is often secreted by a CD4 subset defined as .In the specific case of pertussis vaccines, the complexity of the mechanisms underlying immune protection following vaccination is demonstrated by the observation that equally protective primary vaccinations such as those achieved by whole cell (wP) or acellular (aP) vaccines induce different Th cytokine profiles (3,(6)(7)(9)(10). Particularly, our previous data fr...

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“…9 In human immune-mediated diseases, CD30 is expressed on T cells that serve a regulatory role in rheumatoid arthritis 14 and on cells that accumulate at the inflammatory sites of patients with systemic sclerosis 15,16 and chronic GvHD. 15 Expression of CD30 is detected late after T-cell activation in vitro with immobilized CD3 mAb 17 and activationinduced CD30 is found on T helper 1 (Th1), Th0, and Th2 cell clones. 18,19 CD30 signaling up-regulates the lymph node homing molecule CCR7, 20 provides costimulatory signals to T cells, and enhances their proliferative responses to suboptimal stimulation via T-cell receptor (TCR) engagement.…”

Section: Introductionmentioning

confidence: 99%

Early CD30 signaling is critical for adoptively transferred CD4+CD25+ regulatory T cells in prevention of acute graft-versus-host disease

Zeiser¹,

Nguyen²,

Hou³

et al. 2006

Blood

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IntroductionAcute graft-versus-host disease (aGvHD) is one of the major complications after allogeneic bone marrow transplantation (BMT), which limits the success of this otherwise life-saving strategy. 1 Our group and others have demonstrated that naturally occurring CD4 ϩ CD25 ϩ regulatory T cells (Treg cells) can reduce the incidence and severity of murine aGvHD. [2][3][4][5] In spite of findings that cell-cell contact is critical for Treg-mediated suppression in vitro and that IL-10 production 6 and TGF-␤ surface expression 7 are relevant in vivo, the mechanisms by which Treg cells exert suppressor activity in the setting of aGvHD are poorly understood. Recent reports have described the role of apoptosis induction by activated Treg cells of conventional T cells (Tconv cells) and B cells as a mechanism of suppression. [8][9][10][11][12] The TNF-R superfamily member CD30 has been shown to be expressed on Tr1 regulatory cells that down-modulate nickelspecific immune responses 13 and to be relevant for Treg-mediated protection from allograft rejection. 9 In human immune-mediated diseases, CD30 is expressed on T cells that serve a regulatory role in rheumatoid arthritis 14 and on cells that accumulate at the inflammatory sites of patients with systemic sclerosis 15,16 and chronic GvHD. 15 Expression of CD30 is detected late after T-cell activation in vitro with immobilized CD3 mAb 17 and activationinduced CD30 is found on T helper 1 (Th1), Th0, and Th2 cell clones. 18,19 CD30 signaling up-regulates the lymph node homing molecule CCR7, 20 provides costimulatory signals to T cells, and enhances their proliferative responses to suboptimal stimulation via T-cell receptor (TCR) engagement. 17,21 The ligand for CD30 (CD30L, or CD153) is a membraneassociated glycoprotein related to TNF, 21 which is known to be expressed on thymic epithelial cells (TECs), antigen presenting cells (APCs), activated T cells, neutrophils, eosinophils, and resting B cells. 22,23 CD30-deficient C57B/6 mice display elevated numbers of thymocytes and a gross defect in negative selection, 24 although this was not found in all mouse strains. 25 Overexpression of CD30 on T cells results in augmented thymocyte depletion upon treatment with a superantigen, 26 suggesting an important role for CD30/CD153 interactions in thymic deletion of autoreactive T cells. Recently, the thymic medulla has been demonstrated to be an anatomic site where Treg cells interact with activated dendritic cells (DCs) and Hassall corpuscles 27 that express CD153. 23 In this report, we investigated the role of CD30 signaling in Treg-cell function, demonstrating a critical role for CD30/CD153 interactions early after adoptive transfer. Materials and methods MiceFVB/N (H-2k q , Thy-1.1), C57B/6 (H-2k b , Thy-1.1 or Thy-1.2), C57B/ 6 eGFPϩ , and Balb/c (H-2k d , Thy-1.2) mice were purchased from Jackson Laboratory (Bar Harbor, ME) or Charles River Laboratory (Wilmington, MA). CD30-deficient C57B/6 mice were kindly provided by Dr T. Mak (University of Toronto, ON, Canada); Balb/c...

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In vivo CD30 expression in human diseases with predominant activation of Th2-like T cells

Abstract: Abstract:CD3O is a member of the tumor necrosis factor

Cited by 97 publications

References 21 publications

Genetic factors influencing the development of chronic graft-versus-host disease in a murine model

Genetic factors influencing the development of chronic graft-versus-host disease in a murine model

Soluble CD30 and Lymphocyte Activation Gene-3 (CD223), as Potential Serological Markers of T Helper-Type Cytokine Response Induced by Acellular Pertussis Vaccine

Early CD30 signaling is critical for adoptively transferred CD4+CD25+ regulatory T cells in prevention of acute graft-versus-host disease

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