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Journal articles on the topic 'CD30+/CD30L T cell'

Author: Grafiati

Published: 11 March 2023

Last updated: 19 July 2025

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1

Younes, A., U. Consoli, V. Snell, et al. "CD30 ligand in lymphoma patients with CD30+ tumors." Journal of Clinical Oncology 15, no. 11 (1997): 3355–62. http://dx.doi.org/10.1200/jco.1997.15.11.3355.

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PURPOSE CD30 ligand (CD30L), which is expressed on resting B and activated T lymphocytes, can induce cell death in several CD30+ cell lines. Patients with CD30+ tumors (Hodgkin's disease and Ki-1+ non-Hodgkin's lymphoma) frequently have elevated soluble CD30 (sCD30) levels in their serum, which correlates with a poor prognosis. The role of sCD30 in protecting tumor cells from CD30L-mediated cell death and the pattern of CD30L expression on human peripheral-blood lymphocytes (PBLs) of normal donors and patients with CD30+ tumors are investigated. MATERIALS AND METHODS CD30L surface protein expr

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Willis, Cynthia R., Yi-Ling Hu, Anh Leith, and James B. Rottman. "CD30 / CD30L interactions promote class-switched antibody responses to T-dependent antigens (34.3)." Journal of Immunology 182, no. 1_Supplement (2009): 34.3. http://dx.doi.org/10.4049/jimmunol.182.supp.34.3.

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Abstract The cell-surface glycoproteins CD30 and CD30L are members of the TNFR and TNF superfamilies, respectively. CD30 is expressed on subpopulations of activated T and B cells. CD30L is expressed on activated T cells, macrophages, and dendritic cells, as well as germinal center B cells. CD30 / CD30L interactions provide activation-induced costimulatory signals that sustain T-cell responses, mediate B-cell activity, and generate long-lived memory T cells for chronic B-cell help. Although other activation-induced costimulatory molecules induce antibody isotype class switching, it is less clea

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3

Mori, M., C. Manuelli, N. Pimpinelli, et al. "CD30-CD30 Ligand Interaction in Primary Cutaneous CD30+T-Cell Lymphomas: A Clue to the Pathophysiology of Clinical Regression." Blood 94, no. 9 (1999): 3077–83. http://dx.doi.org/10.1182/blood.v94.9.3077.

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Abstract Primary CD30+ cutaneous T-cell lymphomas (CTCLs) represent a spectrum of non-Hodgkin’s lymphomas (NHLs) that have been well defined at the clinical, histologic, and immunologic level. This group, which includes 2 main entities (large cell lymphoma and lymphomatoid papulosis [LyP]) and borderline cases, is characterized by the expression of CD30 antigen by neoplastic large cells at presentation, possible spontaneous regression of the skin lesions, and generally favorable clinical course. Although the functional relevance of CD30 and its natural ligand (CD30L) expression in most cases o

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Mori, M., C. Manuelli, N. Pimpinelli, et al. "CD30-CD30 Ligand Interaction in Primary Cutaneous CD30+T-Cell Lymphomas: A Clue to the Pathophysiology of Clinical Regression." Blood 94, no. 9 (1999): 3077–83. http://dx.doi.org/10.1182/blood.v94.9.3077.421k28_3077_3083.

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Primary CD30+ cutaneous T-cell lymphomas (CTCLs) represent a spectrum of non-Hodgkin’s lymphomas (NHLs) that have been well defined at the clinical, histologic, and immunologic level. This group, which includes 2 main entities (large cell lymphoma and lymphomatoid papulosis [LyP]) and borderline cases, is characterized by the expression of CD30 antigen by neoplastic large cells at presentation, possible spontaneous regression of the skin lesions, and generally favorable clinical course. Although the functional relevance of CD30 and its natural ligand (CD30L) expression in most cases of NHL is

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5

Barbieri, Alessandro, Marzia Dolcino, Elisa Tinazzi, et al. "Characterization of CD30/CD30L+Cells in Peripheral Blood and Synovial Fluid of Patients with Rheumatoid Arthritis." Journal of Immunology Research 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/729654.

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The CD30/CD30L signalling system has been implicated in the pathogenesis of several autoimmune and inflammatory conditions. In rheumatoid arthritis (RA), soluble CD30 (sCD30) levels reflect the recruitment of CD30+T cells into the inflamed joints and correlate with a positive response to immunosuppressive therapy. The aim of our report was to clarify the role of CD30/CD30L signalling system in the pathogenesis of RA. Our analysis of the CD30L+T cell subsets in peripheral blood (PB) and synovial fluid (SF) of RA patients and of the related cytokine profiles suggests the involvement of CD30/CD30

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6

Rottman, James B., Yi-Ling Hu, and Cynthia Willis. "Blockade of the CD30/CD30L pathway inhibits renal disease in young, SLE-prone NZB/W F1 mice (50.41)." Journal of Immunology 182, no. 1_Supplement (2009): 50.41. http://dx.doi.org/10.4049/jimmunol.182.supp.50.41.

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Abstract CD30 and CD30L are interacting members of the TNFR and TNF family, respectively. CD30 is expressed by subsets of activated T and B cells, whereas CD30L is expressed by subsets of activated T cells, macrophages and dendritic cells. The CD30 / CD30L interaction modulates T cell activation, germinal center formation and antibody isotype class switching. Given the importance of this pathway to B cell function, we tested the hypothesis that blockade of the CD30 / CD30L pathway would decrease or abrogate autoantibody formation and renal disease in the NZB/W F1 murine model of systemic lupus

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7

Romagnani, Paola, Francesco Annunziato, Roberto Manetti, et al. "High CD30 Ligand Expression by Epithelial Cells and Hassal's Corpuscles in the Medulla of Human Thymus." Blood 91, no. 9 (1998): 3323–32. http://dx.doi.org/10.1182/blood.v91.9.3323.

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Abstract CD30 is a member of tumor necrosis factor (TNF) receptor superfamily that is expressed by activated T cells in the presence of interleukin-4 (IL-4). Although CD30 can mediate a variety of signals, CD30-deficient mice have impaired negative selection of T cells, suggesting that at least in the context of murine thymus, CD30 is a cell death–mediating molecule. The ligand for CD30 (CD30L) is a membrane-associated glycoprotein related to TNF, which is known to be expressed mainly by activated T cells and other leukocytes. However, the nature of CD30L-expressing cells involved in the inter

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Romagnani, Paola, Francesco Annunziato, Roberto Manetti, et al. "High CD30 Ligand Expression by Epithelial Cells and Hassal's Corpuscles in the Medulla of Human Thymus." Blood 91, no. 9 (1998): 3323–32. http://dx.doi.org/10.1182/blood.v91.9.3323.3323_3323_3332.

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CD30 is a member of tumor necrosis factor (TNF) receptor superfamily that is expressed by activated T cells in the presence of interleukin-4 (IL-4). Although CD30 can mediate a variety of signals, CD30-deficient mice have impaired negative selection of T cells, suggesting that at least in the context of murine thymus, CD30 is a cell death–mediating molecule. The ligand for CD30 (CD30L) is a membrane-associated glycoprotein related to TNF, which is known to be expressed mainly by activated T cells and other leukocytes. However, the nature of CD30L-expressing cells involved in the interaction wi

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Gattei, Valter, Massimo Degan, Annunziata Gloghini, et al. "CD30 Ligand Is Frequently Expressed in Human Hematopoietic Malignancies of Myeloid and Lymphoid Origin." Blood 89, no. 6 (1997): 2048–59. http://dx.doi.org/10.1182/blood.v89.6.2048.

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Abstract CD30 ligand (CD30L) is a type-II membrane glycoprotein capable of transducing signals leading to either cell death or proliferation through its specific counterstructure CD30. Although several lines of evidence indicate that CD30L plays a key role as a paracrine- or autocrine-acting surface molecule in the deregulated cytokine cascade of Hodgkin's disease, little is known regarding its distribution and biologic significance in other human hematopoietic malignancies. By analyzing tumor cells from 181 patients with RNA studies and immunostaining by the anti-CD30L monoclonal antibody M80

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10

Wiley, S. R., R. G. Goodwin, and C. A. Smith. "Reverse signaling via CD30 ligand." Journal of Immunology 157, no. 8 (1996): 3635–39. http://dx.doi.org/10.4049/jimmunol.157.8.3635.

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Abstract CD30 ligand (CD30L), a member of the TNF family, is a type II membrane protein with a C-terminal extracellular domain that is homologous with the extracellular domains of other TNF family members. Also, like most TNF family members, the N-terminal cytoplasmic domain of CD30L is conserved across species, but not between family members, suggesting a possible biological function. Motivated by this observation, we investigated the potential for CD30L, when activated by cross-linking, to directly transduce a signal to the ligand-bearing cell. Cross-linking of CD30L by a mAb or by CD30-Fc f

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11

Saraiva, Margarida, Philip Smith, Padraic G. Fallon, and Antonio Alcami. "Inhibition of Type 1 Cytokine–mediated Inflammation by a Soluble CD30 Homologue Encoded by Ectromelia (Mousepox) Virus." Journal of Experimental Medicine 196, no. 6 (2002): 829–39. http://dx.doi.org/10.1084/jem.20020319.

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CD30 is up-regulated in several human diseases and viral infections but its role in immune regulation is poorly understood. Here, we report the expression of a functional soluble CD30 homologue, viral CD30 (vCD30), encoded by ectromelia (mousepox) virus, a poxvirus that causes a severe disease related to human smallpox. We show that vCD30 is a 12-kD secreted protein that not only binds CD30L with high affinity and prevents its interaction with CD30, but it also induces reverse signaling in cells expressing CD30L. vCD30 blocked the generation of interferon γ–producing cells in vitro and was a p

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Tsiagbe, Vincent, Eckhard Podack, and Yu Li. "CD30L null SJL mice exhibit reduced lymph node and spleen weights but support growth of transplantable SJL lymphoma RCS-X (48.29)." Journal of Immunology 186, no. 1_Supplement (2011): 48.29. http://dx.doi.org/10.4049/jimmunol.186.supp.48.29.

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Abstract The process by which endogenous retroviral superantigen (vSAg29) expressing SJL lymphomas (RCS) stimulate host CD4+Vβ16+ T cells, in order to elicit help (notably IL-4 and -5) for their growth, has been characterized as “reverse immune surveillance”. This response is facilitated by the high expression of an array of co-stimulating molecules on RCS cells, including B7.1, B7.2, 41BBL, CD40 and CD30. On the basis of their germinal center derivation, SJL lymphomas bear close resemblance to a subpopulation of human germinal center B cell lymphomas, such as CD30+ Hodgkin’s lymphomas. In our

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Rossi, Francesca Maria, Massimo Degan, Linda Mazzocut-Zecchin, et al. "CD30L up-regulates CD30 and IL-4 expression by T cells." FEBS Letters 508, no. 3 (2001): 418–22. http://dx.doi.org/10.1016/s0014-5793(01)03076-9.

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Sethi, Gurupreet, Ashmitaa Logandha Ramamoorthy Premlal, and Michael Croft. "Transient Therapeutic Inhibition of Multiple Costimulatory Molecules Modulates Persistence of Lung Tissue-resident Memory T cells." Journal of Immunology 212, no. 1_Supplement (2024): 0677_7488. http://dx.doi.org/10.4049/jimmunol.212.supp.0677.7488.

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Abstract Costimulatory molecules, crucial for priming of T cells, development of T cell memory, and establishment of inflammatory diseases, have an unknown role in prolonged survival of Tissue-resident memory T (Trm) cells and the maintenance of relapsing inflammation. Single-cell RNA-seq data from asthmatic lungs revealed high expression of OX40, CD30L, and ICOS on CD4 T cells, aligning with transcriptomic analysis of allergen-reactive mouse CD4 Trm cells in a relapsing asthma model. Accordingly, the transient blockade of ICOSL alone or CD30L and OX40L together during tertiary allergen inhala

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15

Gloghini, Annunziata, and Antonino Carbone. "Tumour Microenvironment Contribution to Checkpoint Inhibitor Therapy in Classic Hodgkin Lymphoma." Hemato 5, no. 2 (2024): 199–207. http://dx.doi.org/10.3390/hemato5020016.

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Classic Hodgkin lymphoma (cHL) is a B-cell lymphoma in which tumour cells, the so-called Hodgkin Reed–Sternberg (HRS) cells, are admixed with non-malignant cell types that are a functional part of the disease. Immune cells, fibroblasts, specialised mesenchymal cells, and microvasculature together make up the tumour microenvironment and have functional interactions with tumour cells. HRS cells are surrounded by T and B cells admixed with plasma cells, macrophages, eosinophils, and mast cells. A cross-talk occurs between HRS cells and immune cells of the TME. This cross-talk is mediated either b

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Tang, Ce, Hisakata Yamada, Kensuke Shibata, et al. "A Novel Role of CD30L/CD30 Signaling by T-T Cell Interaction in Th1 Response against Mycobacterial Infection." Journal of Immunology 181, no. 9 (2008): 6316–27. http://dx.doi.org/10.4049/jimmunol.181.9.6316.

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Gruss, HJ, and SK Dower. "Tumor necrosis factor ligand superfamily: involvement in the pathology of malignant lymphomas." Blood 85, no. 12 (1995): 3378–404. http://dx.doi.org/10.1182/blood.v85.12.3378.bloodjournal85123378.

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The TNF receptor superfamily members are all type I membrane glycoproteins with typical homology in the extracellular domain of variable numbers of cysteine-rich repeats (overall homologies, 25% to 30%). In contrast, the TNF ligand superfamily members (with the exception of LT alpha) are type II membrane glycoproteins with homology to TNF in the extracellular domain (overall homologies, 20%). TNF and LT alpha are trimeric proteins and are composed of beta-strands forming a beta-jellyroll. The homology of the beta-strand regions for the TNF ligand superfamily members suggest a similar beta-sand

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18

Ryan, Maureen, Ryan Lyski, Lauren Bou, et al. "SGN-CD30C, an Investigational CD30-Directed Camptothecin Antibody-Drug Conjugate (ADC), Shows Strong Anti Tumor Activity and Superior Tolerability in Preclinical Studies." Blood 136, Supplement 1 (2020): 41–42. http://dx.doi.org/10.1182/blood-2020-136577.

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SGN-CD30C, an investigational CD30-directed ADC, utilizes a potent novel camptothecin derivative as the cytotoxic payload. SGN-CD30C targets the same antigen as brentuximab vedotin (BV), though the payload has a different mechanism of action, namely inhibiting topoisomerase I rather than disrupting microtubules. Unlike monomethyl auristatin E, camptothecin-based therapies do not cause peripheral neuropathy clinically, suggesting that SGN-CD30C may have the potential to avoid one of the most common adverse events associated with BV. In preclinical studies, SGN-CD30C demonstrated strong monother

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19

Akiba, Hisaya, Yasushi Miyahira, Machiko Atsuta, et al. "Critical Contribution of Ox40 Ligand to T Helper Cell Type 2 Differentiation in Experimental Leishmaniasis." Journal of Experimental Medicine 191, no. 2 (2000): 375–80. http://dx.doi.org/10.1084/jem.191.2.375.

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Infection of inbred mouse strains with Leishmania major is a well characterized model for analysis of T helper (Th)1 and Th2 cell development in vivo. In this study, to address the role of costimulatory molecules CD27, CD30, 4-1BB, and OX40, which belong to the tumor necrosis factor receptor superfamily, in the development of Th1 and Th2 cells in vivo, we administered monoclonal antibody (mAb) against their ligands, CD70, CD30 ligand (L), 4-1BBL, and OX40L, to mice infected with L. major. Whereas anti-CD70, anti-CD30L, and anti–4-1BBL mAb exhibited no effect in either susceptible BALB/c or res

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Sethi, Gurupreet Singh, and Michael Croft. "Targeting Multiple Costimulatory Molecules Prevents Persistence of Lung Tissue-resident Memory T cells and Leads to Airway Tolerance." Journal of Immunology 210, no. 1_Supplement (2023): 67.17. http://dx.doi.org/10.4049/jimmunol.210.supp.67.17.

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Abstract Pools of tissue-resident memory T (Trm) cells are thought to maintain and contribute to exacerbations of inflammatory or autoimmune disease. We hypothesized that several costimulatory molecules would control the expansion and maintenance of these populations when responding to antigen, and tested the potential of targeting OX40L, CD30L, and ICOSL, using a house dust mite (HDM) allergen-based mouse model of asthmatic lung inflammation. We found that allergen induced persisting CD4+CD44hiCD62Llo CD69+ and CD69− lung-localized Trm cells and RNA-seq revealed the heterogeneity of these mem

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Alzona, M., H. M. Jäck, R. I. Fisher, and T. M. Ellis. "IL-12 activates IFN-gamma production through the preferential activation of CD30+ T cells." Journal of Immunology 154, no. 1 (1995): 9–16. http://dx.doi.org/10.4049/jimmunol.154.1.9.

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Abstract CD30 is normally expressed by a subset (15 to 20%) of CD45RO+ T cells after activation by a variety of T cell stimuli and defines the principal IFN-gamma-producing T cells subset. Inasmuch as the production of IFN-gamma is regulated by IL-2 and IL-12, we have examined the effects of these cytokines on the proliferation, induction, and function of CD30+ and CD30- T cell subsets. Upon isolation, CD30+CD25+ T cells exhibit high levels of baseline proliferation compared with CD30-CD25+ T cells. Neutralizing Abs specific for IL-2, IL-4, IL-6, or IL-12 had no effect on basal levels of proli

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22

Gilfillan, Molly C., Patricia J. Noel, Eckhard R. Podack, Steven L. Reiner, and Craig B. Thompson. "Expression of the Costimulatory Receptor CD30 Is Regulated by Both CD28 and Cytokines." Journal of Immunology 160, no. 5 (1998): 2180–87. http://dx.doi.org/10.4049/jimmunol.160.5.2180.

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Abstract Costimulation was originally defined and characterized during primary T cell activation. The signaling events that regulate subsequent antigen encounters by T cells are less well defined. In this study we examined the role of CD30 in T cell activation and defined factors that regulate expression of CD30 on T cells. We demonstrate that CD30 expression is restricted to activated T cells and regulated by CD28 signal transduction. In contrast to CD28-expressing TCR Tg cells, CD28-deficient TCR Tg cells did not express CD30 when cultured with peptide and APCs. However, rIL-4 reconstituted

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Alzona, M., H. M. Jäck, R. I. Fisher, and T. M. Ellis. "CD30 defines a subset of activated human T cells that produce IFN-gamma and IL-5 and exhibit enhanced B cell helper activity." Journal of Immunology 153, no. 7 (1994): 2861–67. http://dx.doi.org/10.4049/jimmunol.153.7.2861.

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Abstract CD30 is a lymphoid activation Ag expressed by activated B and T lymphocytes, as well as selected lymphoid malignancies. In T cells, CD30 expression is limited to a minority (15 to 25%) of activated CD45RO+ T cells. Studies were undertaken to define unique functional properties of CD30+ T cells by identifying the profile of cytokine production by CD30+ T cells, and by assessing their ability to provide help for B cell Ig production. Assessment of cytokine mRNA transcripts by reverse transcription-PCR (RT-PCR) revealed the presence of IFN-gamma mRNA transcripts only in CD30+ T cells der

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Lee, S. Y., C. G. Park, and Y. Choi. "T cell receptor-dependent cell death of T cell hybridomas mediated by the CD30 cytoplasmic domain in association with tumor necrosis factor receptor-associated factors." Journal of Experimental Medicine 183, no. 2 (1996): 669–74. http://dx.doi.org/10.1084/jem.183.2.669.

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CD30 is a member of the tumor necrosis factor superfamily and a surface marker for Hodgkin's disease. Normal activated T cells and several virally transformed T or B cell lines also show CD30 expression. The interaction of CD30 with its ligand induces cell death or proliferation, depending on the cell type. In this report we characterize the signals mediated by the intracellular domain of CD30 and show that, in combination with signal(s) transduced by the T cell receptor, the multimerization of CD30 cytoplasmic domain induces Fas(CD95)-independent cell death in T cell hybridomas. Deletion anal

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Martin, James M., Hong Wu, and Stefan K. Barta. "CD30+ T-cell lymphoproliferative disorders." Chinese Clinical Oncology 8, no. 1 (2019): 4. http://dx.doi.org/10.21037/cco.2018.09.06.

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Sato, Keisuke, Tomohiro Kozako, Akira Nakano, et al. "Extracellular CD30 and ADAM10/17 Regulate Brentuximab Vedotin-Induced Cell Death in an Adult T-Cell Leukemia Cell Line." Blood 142, Supplement 1 (2023): 5803. http://dx.doi.org/10.1182/blood-2023-173221.

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Adult T-cell leukemia/lymphoma (ATL) is a human T-cell leukemia virus 1 (HTLV-1)-induced malignancy of mature T lymphocytes with poor outcomes. Brentuximab vedotin (BV), which is an anti-CD30 antibody conjugated with monomethyl auristatin E, is included in the treatment of CD30-positive ATL, but there is no useful therapeutic marker for BV. Soluble CD30 (sCD30) in serum is increased in aggressive-type ATL at diagnosis, but the effects of extracellular CD30 on BV-induced cell death in ATL remain unclear. Similarly, a disintegrin and metalloproteinase (ADAM) 10 and 17 have CD30 sheddase activity

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Carbone, Antonino, Annunziata Gloghini, Gianluca Gaidano, Riccardo Dalla-Favera, and Brunangelo Falini. "BCL-6 Protein Expression in Human Peripheral T-Cell Neoplasms Is Restricted to CD30+ Anaplastic Large-Cell Lymphomas." Blood 90, no. 6 (1997): 2445–50. http://dx.doi.org/10.1182/blood.v90.6.2445.

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Abstract The expression pattern of the BCL-6 transcription factor has been assessed in normal and neoplastic B-cell populations and in Hodgkin's disease. However, little is known about BCL-6 expression and its biological significance in T-cell neoplasms. In this study, a series of 59 lymphoma samples, including 27 CD30+ anaplastic large-cell lymphomas (ALCLs), 24 other peripheral T-cell neoplasms, and 8 T-cell lymphoblastic lymphomas (T-LBLs), as well as a panel of t(2; 5)-positive lymphoma-derived human cell lines, were evaluated for BCL-6 protein expression by immunohistochemistry on frozen

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Carbone, Antonino, Annunziata Gloghini, Gianluca Gaidano, Riccardo Dalla-Favera, and Brunangelo Falini. "BCL-6 Protein Expression in Human Peripheral T-Cell Neoplasms Is Restricted to CD30+ Anaplastic Large-Cell Lymphomas." Blood 90, no. 6 (1997): 2445–50. http://dx.doi.org/10.1182/blood.v90.6.2445.2445_2445_2450.

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The expression pattern of the BCL-6 transcription factor has been assessed in normal and neoplastic B-cell populations and in Hodgkin's disease. However, little is known about BCL-6 expression and its biological significance in T-cell neoplasms. In this study, a series of 59 lymphoma samples, including 27 CD30+ anaplastic large-cell lymphomas (ALCLs), 24 other peripheral T-cell neoplasms, and 8 T-cell lymphoblastic lymphomas (T-LBLs), as well as a panel of t(2; 5)-positive lymphoma-derived human cell lines, were evaluated for BCL-6 protein expression by immunohistochemistry on frozen sections

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Gruss, HJ, N. Boiani, DE Williams, RJ Armitage, CA Smith, and RG Goodwin. "Pleiotropic effects of the CD30 ligand on CD30-expressing cells and lymphoma cell lines." Blood 83, no. 8 (1994): 2045–56. http://dx.doi.org/10.1182/blood.v83.8.2045.2045.

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Abstract CD30 is a member of the tumor necrosis factor receptor superfamily. CD30 was originally described as a cell surface antigen on primary and cultured Hodgkin's and Reed-Sternberg cells. In this study, recombinant human CD30 ligand was expressed on the surface of CV-1/EBNA cells and tested for biologic activities on a variety of different CD30+ human lymphoma cell lines. CD30 ligand enhanced Ig secretion of Epstein-Barr virus (EBV)-immortalized, CD30+ lymphoblastoid B-cell lines, but not Burkitt lymphoma lines. Recombinant CD30 ligand enhanced proliferation of “T-cell-like” Hodgkin's dis

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Gruss, HJ, N. Boiani, DE Williams, RJ Armitage, CA Smith, and RG Goodwin. "Pleiotropic effects of the CD30 ligand on CD30-expressing cells and lymphoma cell lines." Blood 83, no. 8 (1994): 2045–56. http://dx.doi.org/10.1182/blood.v83.8.2045.bloodjournal8382045.

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CD30 is a member of the tumor necrosis factor receptor superfamily. CD30 was originally described as a cell surface antigen on primary and cultured Hodgkin's and Reed-Sternberg cells. In this study, recombinant human CD30 ligand was expressed on the surface of CV-1/EBNA cells and tested for biologic activities on a variety of different CD30+ human lymphoma cell lines. CD30 ligand enhanced Ig secretion of Epstein-Barr virus (EBV)-immortalized, CD30+ lymphoblastoid B-cell lines, but not Burkitt lymphoma lines. Recombinant CD30 ligand enhanced proliferation of “T-cell-like” Hodgkin's disease-deri

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Ellis, T. M., P. E. Simms, D. J. Slivnick, H. M. Jäck, and R. I. Fisher. "CD30 is a signal-transducing molecule that defines a subset of human activated CD45RO+ T cells." Journal of Immunology 151, no. 5 (1993): 2380–89. http://dx.doi.org/10.4049/jimmunol.151.5.2380.

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Abstract CD30 has been extensively studied as a cell surface marker expressed by Reed-Sternberg cells of Hodgkin's disease and other hematologic malignancies, although little is known about its expression by normal lymphoid cells. We therefore characterized the requirements for the induction of CD30 expression and identified the subsets of T cells that express CD30. CD30 is inducible on approximately 15% of normal PBMC stimulated with any of a variety of nonspecific T cell activators, including PHA, Con A, anti-T11(2) + T11(3), and anti-CD3; ionomycin alone induced lower percentages of CD30+ T

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Chen, Yi-Bin, Sean McDonough, Robert Hasserjian, et al. "Expression of CD30 in patients with acute graft-versus-host disease." Blood 120, no. 3 (2012): 691–96. http://dx.doi.org/10.1182/blood-2012-03-415422.

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Abstract Acute GVHD (aGVHD) remains a major source of morbidity after allogeneic hematopoietic cell transplantation. CD30 is a cell-surface protein expressed on certain activated T cells. We analyzed CD30 expression on peripheral blood T-cell subsets and soluble CD30 levels in 26 patients at the time of presentation of aGVHD, before the initiation of treatment, compared with 27 patients after hematopoietic cell transplantation without aGVHD (NONE). Analysis by flow cytometry showed that patients with aGVHD had a greater percentage of CD30 expressing CD8+ T cells with the difference especially

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Nakashima, Makoto, and Kaoru Uchimaru. "CD30 Expression and Its Functions during the Disease Progression of Adult T-Cell Leukemia/Lymphoma." International Journal of Molecular Sciences 24, no. 10 (2023): 8731. http://dx.doi.org/10.3390/ijms24108731.

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CD30, a member of the tumor necrosis factor receptor superfamily, plays roles in pro-survival signal induction and cell proliferation in peripheral T-cell lymphoma (PTCL) and adult T-cell leukemia/lymphoma (ATL). Previous studies have identified the functional roles of CD30 in CD30-expressing malignant lymphomas, not only PTCL and ATL, but also Hodgkin lymphoma (HL), anaplastic large cell lymphoma (ALCL), and a portion of diffuse large B-cell lymphoma (DLBCL). CD30 expression is often observed in virus-infected cells such as human T-cell leukemia virus type 1 (HTLV-1). HTLV-1 is capable of imm

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de Leval, Laurence, David S. Rickman, Caroline Thielen, et al. "The gene expression profile of nodal peripheral T-cell lymphoma demonstrates a molecular link between angioimmunoblastic T-cell lymphoma (AITL) and follicular helper T (TFH) cells." Blood 109, no. 11 (2007): 4952–63. http://dx.doi.org/10.1182/blood-2006-10-055145.

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Abstract The molecular alterations underlying the pathogenesis of angioimmunoblastic T-cell lymphoma (AITL) and peripheral T-cell lymphoma, unspecified (PTCL-u) are largely unknown. In order to characterize the ontogeny and molecular differences between both entities, a series of AITLs (n = 18) and PTCLs-u (n = 16) was analyzed using gene expression profiling. Unsupervised clustering correlated with the pathological classification and with CD30 expression in PTCL-u. The molecular profile of AITLs was characterized by a strong microenvironment imprint (overexpression of B-cell– and follicular d

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Del Prete, G., M. De Carli, M. M. D'Elios, et al. "CD30-mediated signaling promotes the development of human T helper type 2-like T cells." Journal of Experimental Medicine 182, no. 6 (1995): 1655–61. http://dx.doi.org/10.1084/jem.182.6.1655.

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We have recently shown that CD30, a member of the tumor necrosis factor/nerve growth factor receptor superfamily, is preferentially expressed by human T cell clones producing T helper (Th) type 2 cytokines. We report here that costimulation with an agonistic anti-CD30 monoclonal antibody enhanced antigen (Ag)-induced proliferation and cytokine secretion by established human Th2 and Th0 clones. Moreover, costimulation of peripheral blood mononuclear cells with the same anti-CD30 monoclonal antibody resulted in the preferential development of Ag-specific T cell lines and clones showing a Th2-lik

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Agrawal, B., M. Reddish, and B. M. Longenecker. "CD30 expression on human CD8+ T cells isolated from peripheral blood lymphocytes of normal donors." Journal of Immunology 157, no. 8 (1996): 3229–34. http://dx.doi.org/10.4049/jimmunol.157.8.3229.

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Abstract By direct or indirect immunofluorescence using FITC as a fluorochrome, 0 to 2% of the T cells isolated from peripheral blood of normal healthy individuals was found to be CD30+. Using indirect immunofluorescence and phycoerythrin-labeled Ab, higher percentages of CD30+ T cells (3-31%) were repeatedly found in the peripheral blood of normal healthy donors. The majority (85-90%) of CD30+ T cells obtained from PBLs of normal healthy donors were found in the CD8+ cell population. Following FACS sorting of the T cell populations into CD30+ and CD30- subpopulations, approximately 85 to 90%

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Aneja, Amandeep, Raghava LevakaVeera, Viren Patel, and Ashish Bains. "Aggressive Subcutaneous Panniculitis-Like CD30+ Peripheral T-Cell Lymphoma with Diffuse EBER Expression." Case Reports in Hematology 2014 (2014): 1–4. http://dx.doi.org/10.1155/2014/874725.

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T-cell lineage lymphoma with an intense membranous and paranuclear CD30 expression in the absence of ALK1 raises a differential diagnosis of peripheral T-cell lymphoma (PTCL), NOS and anaplastic large cell lymphoma (ALCL), ALK negative. However, Epstein-Barr virus is consistently negative in ALCL and is not considered an implicating factor in its pathogenesis. We describe a case of T-cell lymphoma showing anaplastic large cell morphology with scattered hallmark cells and a uniform CD30 and Epstein-Barr virus encoded early RNA (EBER) expression that primarily involved the subcutaneous tissue at

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Prator, Cecilia A., Cassandra Thanh, Shreya Kumar, et al. "Circulating CD30+CD4+ T Cells Increase Before Human Immunodeficiency Virus Rebound After Analytical Antiretroviral Treatment Interruption." Journal of Infectious Diseases 221, no. 7 (2019): 1146–55. http://dx.doi.org/10.1093/infdis/jiz572.

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Abstract Background Identification of nonviral markers of human immunodeficiency virus (HIV) infection that increase before viral rebound during analytical treatment interruption (ATI) may affect HIV persistence research. We previously showed that HIV ribonucleic acid (RNA) is enriched in CD30+CD4+ T cells in many individuals. Here, we studied CD30+CD4+ T-cell dynamics before ATI, during ATI (before detectable plasma RNA), and after HIV rebound. Methods Peripheral blood mononuclear cells from 23 participants collected longitudinally from 5 Adult AIDS Clinical Trials Group studies incorporating

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Steinhoff, Matthias, Michael Hummel, Ioannis Anagnostopoulos, et al. "Single-cell analysis of CD30+ cells in lymphomatoid papulosis demonstrates a common clonal T-cell origin." Blood 100, no. 2 (2002): 578–84. http://dx.doi.org/10.1182/blood-2001-12-0199.

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Abstract Lymphomatoid papulosis (LyP) represents an intriguing cutaneous T-cell lymphoproliferative disorder with a histologic appearance resembling malignant lymphoma. This finding strongly contrasts with the benign clinical course of the disease. However, in 10% to 20% of cases, LyP can precede, coexist with, or follow malignant lymphoma. In these cases, the same T-cell population has been shown to be present in the LyP as well as in the associated lymphoma. In most LyP cases, there is—despite the sometimes extremely long course of the disease—no evolution of a secondary lymphoma. The invest

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de Leval, Laurence, David Rickman, Caroline Thielen, et al. "The Gene Expression Profile of Nodal T-Cell Lymphomas Identifies a Molecular Link between Angioimmunoblastic T-Cell Lymphoma (AITL) and Follicular Helper T Cells (TFH), and between CD30+ Peripheral T-Cell Lymphoma and ALK-Negative Anaplastic Large Cell Lymphoma (ALCL)." Blood 108, no. 11 (2006): 289. http://dx.doi.org/10.1182/blood.v108.11.289.289.

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Abstract AITL and PTCL-U, the two most common forms of T-cell lymphomas in western countries, usually present as nodal disease and pursue an aggressive clinical course. AITL is commonly associated with a constellation of clinical symptoms and distinct pathological features. Conversely, PTCL-U lacks precise diagnostic criteria, and by default comprises cases not fulfilling criteria for other entities, including tumors with borderline features to ALCL and AITL. The genetic alterations and pathogenic mechanisms underlying AITL and PTCL-U are largely unknown. To determine whether the molecular sig

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Lezama, Lhara Sumarriva, and Dita Gratzinger. "Nodal Involvement by CD30+ Cutaneous Lymphoproliferative Disorders and Its Challenging Differentiation From Classical Hodgkin Lymphoma." Archives of Pathology & Laboratory Medicine 142, no. 1 (2018): 139–42. http://dx.doi.org/10.5858/arpa.2016-0352-rs.

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Primary cutaneous lymphomas are defined as non-Hodgkin lymphomas that present in the skin with no evidence of extracutaneous disease at the time of diagnosis. Mycosis fungoides is the most common type of primary cutaneous T-cell lymphoma, representing almost 50% of primary cutaneous T-cell lymphomas, and primary cutaneous CD30+ T-cell lymphoproliferative disorders are the second most common group (30%). Transformed mycosis fungoides is usually CD30+ and can involve multiple nodal sites; other primary cutaneous CD30+ T-cell lymphoproliferative disorders can also involve draining regional nodes.

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Grogan, Bryan, Reice James, Michelle Ulrich, Shyra Gardai, Ryan Heiser, and Reice James. "696 Brentuximab vedotin, a CD30-directed antibody-drug conjugate, selectively depletes activated Tregs in vitro and in vivo." Journal for ImmunoTherapy of Cancer 8, Suppl 3 (2020): A738. http://dx.doi.org/10.1136/jitc-2020-sitc2020.0696.

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BackgroundRegulatory T cells (Tregs) play an important role in maintaining immune homeostasis, preventing excessive inflammation in normal tissues. In cancer, Tregs hamper anti-tumor immunosurveillance and facilitate immune evasion. Selective targeting of intratumoral Tregs is a potentially promising treatment approach. Orthogonal evaluation of tumor-infiltrating lymphocytes (TILs) in solid tumors in mice and humans have identified CCR8, and several tumor necrosis family receptors (TNFRs), including TNFSFR8 (CD30), as receptors differentially upregulated on intratumoral Tregs compared to norma

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Advani, Ranjana H., Steven M. Horwitz, Swaminathan Padmanabhan Iyer, et al. "Response to A+CHP by CD30 expression in the ECHELON-2 trial." Journal of Clinical Oncology 37, no. 15_suppl (2019): 7538. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.7538.

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7538 Background: Brentuximab vedotin (BV) is an antibody-drug conjugate that targets CD30. The ECHELON-2 (E-2) study demonstrated significantly longer progression-free and overall survival with BV plus cyclophosphamide, doxorubicin, and prednisone (A+CHP) versus CHOP in frontline treatment of patients (pts) with CD30+ peripheral T-cell lymphoma (PTCL). Complete remission (CR) rate (A+CHP 68%; CHOP 56%) and objective response rate (ORR) (A+CHP 83%; CHOP 72%) were also significantly increased. Expression of CD30 is universal in systemic anaplastic large-cell lymphoma (sALCL) but variable among n

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Hutchison, R. E., C. W. Berard, J. J. Shuster, M. P. Link, T. E. Pick, and S. B. Murphy. "B-cell lineage confers a favorable outcome among children and adolescents with large-cell lymphoma: a Pediatric Oncology Group study." Journal of Clinical Oncology 13, no. 8 (1995): 2023–32. http://dx.doi.org/10.1200/jco.1995.13.8.2023.

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PURPOSE The goal of this study was to assess the immunophenotype of uniformly treated cases of pediatric large-cell non-Hodgkin's lymphoma (NHL) to determine the prognostic importance of B-cell and T-cell lineages and of CD30 positivity. PATIENTS AND METHODS Sixty-nine patients were analyzed by immunochemistry. All patients were classified histologically, staged in a uniform manner, and treated according to one of two protocols for localized (stage I and II) NHL or advanced (stage III and IV) large-cell NHL. Antibodies included anti-CD45, CD20, CD45Ra, MB-2 (not clustered), CD3, CD45Ro, CD43,

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Fukamachi, Shoko, Kazunari Sugita, Yu Sawada, Toshinori Bito, Motonobu Nakamura, and Yoshiki Tokura. "Drug-induced CD30+ T cell pseudolymphoma." European Journal of Dermatology 19, no. 3 (2009): 292–94. http://dx.doi.org/10.1684/ejd.2009.0667.

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Estrada, S., and W. Anderson. "CD30-Positive Peripheral T-Cell Lymphoma." Journal of Cutaneous Pathology 32, no. 1 (2008): 86. http://dx.doi.org/10.1111/j.0303-6987.2005.320bq.x.

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Sandlund, J. T., C. H. Pui, V. M. Santana, et al. "Clinical features and treatment outcome for children with CD30+ large-cell non-Hodgkin's lymphoma." Journal of Clinical Oncology 12, no. 5 (1994): 895–98. http://dx.doi.org/10.1200/jco.1994.12.5.895.

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PURPOSE To determine the frequency of CD30 expression and its relationship to clinical features, immunophenotype, histotype, and outcome in childhood large-cell non-Hodgkin's lymphoma (NHL). PATIENTS AND METHODS We reviewed 45 cases of large-cell NHL in children treated at St Jude Children's Research Hospital from 1975 to 1990 for whom there was sufficient tissue to perform immunophenotypic studies. All 45 were screened with a panel of antibodies to detect the presence of CD30 and T-cell and B-cell antigens. Cases were classified according to the National Cancer Institute (NCI) Working Formula

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Manetti, R., F. Annunziato, R. Biagiotti, et al. "CD30 expression by CD8+ T cells producing type 2 helper cytokines. Evidence for large numbers of CD8+CD30+ T cell clones in human immunodeficiency virus infection." Journal of Experimental Medicine 180, no. 6 (1994): 2407–11. http://dx.doi.org/10.1084/jem.180.6.2407.

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A large panel of CD8+ T cell clones generated from peripheral blood lymphocytes (PBL) of healthy donors or human immunodeficiency virus (HIV)-infected individuals were assessed for both cytokine secretion profile and CD30 expression and release. The great majority of CD8+ T cell clones generated from healthy individuals showed the ability to produce interferon gamma (IFN-gamma), but not interleukin 4 (IL-4), and none of them either expressed membrane CD30 or released substantial amounts of soluble CD30 (sCD30) in their supernatant. In contrast, high numbers of CD8+ T cell clones generated from

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Nakamura, T., R. K. Lee, S. Y. Nam, et al. "Reciprocal regulation of CD30 expression on CD4+ T cells by IL-4 and IFN-gamma." Journal of Immunology 158, no. 5 (1997): 2090–98. http://dx.doi.org/10.4049/jimmunol.158.5.2090.

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Abstract Prior studies have implicated CD30 as a marker for Th2 cells, but the mechanism that underlies this correlation was unknown. We show here that CD30 was expressed on activated CD4+ T cells in the presence of IL-4. In the absence of endogenously produced IL-4, however, even Th2 lineage cells lost CD30 expression. Thus, CD30 is not an intrinsic marker of Th2 cells, but is inducible by IL-4. CD30 was also found to be down-regulated by IFN-gamma. Committed Th1 effector cells do not express CD30, although differentiating Th1 lineage cells temporarily express CD30. The transient expression o

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Voorhees, Timothy J., Natalie S. Grover, Anne Beaven, et al. "Retrospective Cohort Study Analyzing the Safety and Efficacy of Anti-PD-1 Therapy Following CD30 CAR-T Cell Therapy in Relapsed/Refractory Hodgkin Lymphoma." Blood 134, Supplement_1 (2019): 3233. http://dx.doi.org/10.1182/blood-2019-122846.

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Background: The safety and efficacy of treating pts with relapsed/refractory (r/r) CD30+ lymphomas with chimeric receptor modified T cells targeting the CD30 molecule (CD30.CAR-T) has been recently demonstrated (Grover et al., ASH 2018). Expression of PD-1 on CD30.CAR-T cells has been observed post-infusion at the time of disease recurrence. To determine the safety and efficacy of anti-PD-1 mAb therapy (CPI) post CD30.CAR-T cell therapy, we present a retrospective cohort review of pts with r/r Hodgkin lymphoma (HL) who subsequently received CPI after CD30.CAR-T progression. Methods: We followe

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