Relevant bibliographies by topics / CD30L T cell

Academic literature on the topic 'CD30L T cell'

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Published: 11 March 2023

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Journal articles on the topic "CD30L T cell"

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Younes, A., U. Consoli, V. Snell, K. Clodi, K. O. Kliche, J. L. Palmer, H. J. Gruss, et al. "CD30 ligand in lymphoma patients with CD30+ tumors." Journal of Clinical Oncology 15, no. 11 (November 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 expression was determined by two-color flow cytometry on PBLs of patients with CD30+ tumors and normal individuals. CD30L levels were determined on subsets of PBLs before and after stimulation with phytohemagglutinin (PHA), anti-CD3 antibody, or CD40L. sCD30 was measured by enzyme-linked immunosorbent assay (ELISA). The apoptotic activity of membrane-bound CD30L was tested in a CD30+ cell line by the annexin V-binding method. RESULTS Unstimulated T lymphocytes of normal donors and patients with lymphoma rarely expressed CD30L surface protein, but were able to express it after stimulation with PHA or anti-CD3 antibody. Resting B cells of patients with CD30+ tumors had lower levels of detectable surface CD30L compared with normal donors (mean, 55% and 80.6%, respectively; P = .0008). Patients with high levels of serum sCD30 had lower detectable levels of CD30L on their PBLs (R2 = .72, P = .0008) and exogenous sCD30 blocked membrane-bound CD30L-mediated apoptosis in a CD30+ cell line. CONCLUSION In patients with CD30+ tumors, sCD30 can decrease the availability of CD30L on PBLs. Blocking the apoptosis-inducing activity of CD30L by its soluble receptor may explain how CD30+ tumors escape immunosurveillance and may be related to the reported poor prognosis of patients who have elevated sCD30 levels.
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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 (April 1, 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 clear what the function is of CD30 signaling on class switching and antibody production. Therefore, we tested the effect of in vivo blockade of the CD30 / CD30L pathway on antibody class switching in response to T-dependent antigens using two systems that require activated-T cells to stimulate B-cell responses. First, BALB/c mice immunized with a T-dependent antigen and treated with anti-CD30L antibodies produced less antigen-specific antibodies of IgG1 and IgE isotypes as compared to control-treated mice, whereas antigen-specific antibodies of the IgM isotype were similar in all groups. Likewise, NZB/W F1 lupus-prone mice treated with anti-CD30L antibodies produced less anti-dsDNA antibodies of the IgG1 and IgG2a isotypes as compared to control-treated mice, whereas anti-dsDNA antibodies of the IgM isotype were similar in all groups. In both systems, specific subpopulations of lymphocytes necessary for responses to T-dependent antigens were reduced by blockade of the CD30 / CD30L pathway. Our results demonstrate that CD30 / CD30L interactions positively regulate T-cell dependent B-cell responses necessary for class-switched antibody responses.
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Mori, M., C. Manuelli, N. Pimpinelli, C. Mavilia, E. Maggi, M. Santucci, B. Bianchi, P. Cappugi, B. Giannotti, and M. E. Kadin. "CD30-CD30 Ligand Interaction in Primary Cutaneous CD30+T-Cell Lymphomas: A Clue to the Pathophysiology of Clinical Regression." Blood 94, no. 9 (November 1, 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 of NHL is presently undefined, previous studies indicate that CD30L is likely to mediate reduction of proliferation in CD30+ anaplastic large-cell NHL. No information is currently available concerning the expression of CD30L in primary CD30+ CTCLs. In this study, we investigated the immunophenotypic and genotypic expression of CD30 and CD30L in different developmental phases of skin lesions (growing v spontaneously regressing). By immunohistochemistry, CD30L expression was detected in regressing lesions only; by molecular analysis, the expression of CD30L was clearly higher in regressing lesions than in growing ones. CD30L, while expressed by some small lymphocytes, was most often coexpressed by CD30+neoplastic large cells, as demonstrated by 2-color immunofluorescence and by immunohistochemistry on paraffin sections. Taken together, these data suggest that CD30-CD30L interaction may play a role in the pathobiology of primary cutaneous CD30+lymphoproliferative disorders. In particular, CD30L (over)expression might have a major role in the mechanism of self-regression of skin lesions, the most distinctive clinical feature of this cutaneous lymphoma subtype.
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Mori, M., C. Manuelli, N. Pimpinelli, C. Mavilia, E. Maggi, M. Santucci, B. Bianchi, P. Cappugi, B. Giannotti, and M. E. Kadin. "CD30-CD30 Ligand Interaction in Primary Cutaneous CD30+T-Cell Lymphomas: A Clue to the Pathophysiology of Clinical Regression." Blood 94, no. 9 (November 1, 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 presently undefined, previous studies indicate that CD30L is likely to mediate reduction of proliferation in CD30+ anaplastic large-cell NHL. No information is currently available concerning the expression of CD30L in primary CD30+ CTCLs. In this study, we investigated the immunophenotypic and genotypic expression of CD30 and CD30L in different developmental phases of skin lesions (growing v spontaneously regressing). By immunohistochemistry, CD30L expression was detected in regressing lesions only; by molecular analysis, the expression of CD30L was clearly higher in regressing lesions than in growing ones. CD30L, while expressed by some small lymphocytes, was most often coexpressed by CD30+neoplastic large cells, as demonstrated by 2-color immunofluorescence and by immunohistochemistry on paraffin sections. Taken together, these data suggest that CD30-CD30L interaction may play a role in the pathobiology of primary cutaneous CD30+lymphoproliferative disorders. In particular, CD30L (over)expression might have a major role in the mechanism of self-regression of skin lesions, the most distinctive clinical feature of this cutaneous lymphoma subtype.
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Gattei, Valter, Massimo Degan, Annunziata Gloghini, Angela De Iuliis, Salvatore Improta, Francesca Maria Rossi, Donatella Aldinucci, et al. "CD30 Ligand Is Frequently Expressed in Human Hematopoietic Malignancies of Myeloid and Lymphoid Origin." Blood 89, no. 6 (March 15, 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, we were able to show that human hematopoietic malignancies of different lineage and maturation stage display a frequent and broad expression of the ligand. CD30L mRNA and surface protein were detected in 60% of acute myeloid leukemias (AMLs), 54% of B-lineage acute lymphoblastic leukemias (ALLs), and in a consistent fraction (68%) of B-cell lymphoproliferative disorders. In this latter group, hairy cell leukemia and high-grade B-cell non-Hodgkin's lymphoma (B-NHL) expressed a higher surface density of CD30L as compared with B-cell chronic lymphocytic leukemia and low-grade B-NHL. Purified plasmacells from a fraction of multiple myeloma patients also displayed CD30L mRNA and protein. A more restricted expression of CD30L was found in T-cell tumors that was mainly confined to neoplasms with an activated peripheral T-cell phenotype, such as T-cell prolymphocytic leukemia, peripheral T-NHL, and adult T-cell leukemia/lymphoma. In contrast, none of the T-lineage ALLs analyzed expressed the ligand. In AML, a high cellular density of CD30L was detected in French-American-British M3, M4, and M5 phenotypes, which are directly associated with the presence on tumor cells of certain surface structures, including the p55 interleukin-2 receptor α-chain, the αM (CD11b) chain of β2 integrins, and the intercellular adhesion molecule-1 (CD54). Analysis of normal hematopoietic cells evidenced that, in addition to circulating and tonsil B cells, a fraction of bone marrow myeloid precursors, erythroblasts, and subsets of megakaryocytes also express CD30L. Finally, we have shown that native CD30L expressed on primary leukemic cells is functionally active by triggering both mitogenic and antiproliferative signals on CD30+ target cells. As opposed to CD30L, only 10 of 181 primary tumors expressed CD30 mRNA or protein, rendering therefore unlikely a CD30-CD30L autocrine loop in human hematopoietic neoplasms. Taken together, our data indicate that CD30L is widely expressed from early to late stages of human hematopoiesis and suggest a regulatory role for this molecule in the interactions of normal and malignant hematopoietic cells with CD30+ immune effectors and/or microenvironmental accessory cells.
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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 (April 1, 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 erythematosis (SLE). Young (5 mo) NZB/W F1 mice were treated with 300 μg CD30L blocking (M15-N297A) or blocking / depleting (M15-IgG2a) antibody weekly for 3 months during the onset of autoimmunity. Both treatments a) reduced the onset and severity of proteinuria, b) significantly decreased the severity of renal histologic scores, c) decreased glomerular immune complex and complement deposition and d) these effects were associated with reduced production of anti-DNA antibodies of the IgG, but not IgM isotype. CD30 / CD30L blockade may be a viable approach for the treatment of SLE.
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Barbieri, Alessandro, Marzia Dolcino, Elisa Tinazzi, Antonella Rigo, Giuseppe Argentino, Giuseppe Patuzzo, Andrea Ottria, Ruggero Beri, Antonio Puccetti, and Claudio Lunardi. "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/CD30L signalling in polarization of T cells towards a Th17 phenotype with proinflammatory features. Moreover, in RA SF nearly 50% of Treg cells express CD30, probably as an attempt to downmodulate the ongoing inflammation. We also show here that the engagement of CD30L on neutrophils stimulated with CD30/Fc chimera may play a crucial role in RA inflammation since activated neutrophils release IL-8, thus potentially amplifying the local inflammatory damage. In conclusion, the results obtained suggest that the complex CD30/CD30L signalling pathway is implicated in the pathogenesis and progression of RA synovitis through a concerted action on several immune effector cells.
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Romagnani, Paola, Francesco Annunziato, Roberto Manetti, Carmelo Mavilia, Laura Lasagni, Cinzia Manuelli, Gabriella B. Vannelli, et al. "High CD30 Ligand Expression by Epithelial Cells and Hassal's Corpuscles in the Medulla of Human Thymus." Blood 91, no. 9 (May 1, 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 interaction with CD30+ thymocytes is unclear. We report here that in postnatal human thymus the great majority of CD30+ cells are double positive (CD4+CD8+), activated, IL-4 receptor–expressing T cells which selectively localize in the medullary areas. Moreover, many medullary epithelial cells and Hassal's corpuscles in the same thymus specimens showed unusually high expression of CD30L in comparison with other lymphoid or nonlymphoid tissues. These findings provide additional information on the nature and localization of CD30+ thymocytes and show that epithelial cells are the major holder of CD30L in the thymic medulla.
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Romagnani, Paola, Francesco Annunziato, Roberto Manetti, Carmelo Mavilia, Laura Lasagni, Cinzia Manuelli, Gabriella B. Vannelli, et al. "High CD30 Ligand Expression by Epithelial Cells and Hassal's Corpuscles in the Medulla of Human Thymus." Blood 91, no. 9 (May 1, 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 with CD30+ thymocytes is unclear. We report here that in postnatal human thymus the great majority of CD30+ cells are double positive (CD4+CD8+), activated, IL-4 receptor–expressing T cells which selectively localize in the medullary areas. Moreover, many medullary epithelial cells and Hassal's corpuscles in the same thymus specimens showed unusually high expression of CD30L in comparison with other lymphoid or nonlymphoid tissues. These findings provide additional information on the nature and localization of CD30+ thymocytes and show that epithelial cells are the major holder of CD30L in the thymic medulla.
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Wiley, S. R., R. G. Goodwin, and C. A. Smith. "Reverse signaling via CD30 ligand." Journal of Immunology 157, no. 8 (October 15, 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 fusion protein induced the production of IL-8 by freshly isolated neutrophils. Further, both cross-linking mechanisms produced a rapid oxidative burst. Indirect effects through CD30 were ruled out, since CD30L, but not CD30, is expressed on neutrophils. Expression of CD30L can be induced in peripheral blood T cells by cross-linking the CD3 component of the TCR. Peripheral blood T cells exposed to suboptimal concentrations of anti-CD3 increased metabolic activity, proliferated, and produced IL-6 in response to cross-linking of CD30L. These results indicate that cross-linked CD30L can transduce a signal to the ligand-bearing cell. This "reverse signaling" via CD30L taken together with previously published data concerning other ligands in the TNF family strongly suggest that, as a rule, TNF family members and their cognate receptors signal bidirectionally, blurring the distinction between ligand and receptor.
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Dissertations / Theses on the topic "CD30L T cell"

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Mühle, Kerstin. "Interaction of CD8+CD40L+ T cells with B cells." Doctoral thesis, Humboldt-Universität zu Berlin, 2018. http://dx.doi.org/10.18452/19127.

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ZTLs vermitteln die Eliminierung von infizierten und entarteten Zellen durch Apoptose. Neuste Erkenntnisse unserer Gruppe haben gezeigt, dass eine Subpopulation der CD8+ T-Zellen, anstelle der zytotoxischen Marker das Oberflächenmolekül CD40L exprimiert. Die Expression von CD40L ist bislang als Schlüsselmolekül für die CD4+ T-Zell vermittelte Hilfe bekannt, welche durch Bindung an den CD40 Rezeptor auf anderen Immunzellen induziert wird. Das von den CD4+ T–Zellen ausgehende CD40L Signal ist besonders für die T-Zell abhängige B-Zell Aktivierung und die Bildung von Keimzentren essentiell, in denen B-Zellen heranreifen und hochaffine Antikörper produzieren um den Organismus vor eindringenden Erregern zu schützen. Aufgrund der CD40L-assoziierten Helferfunktion sollte in dieser Arbeit untersucht werden, welche Auswirkungen die Interaktion von CD8+CD40L+ T-Zellen mit B Zellen hat. In in vitro Studien konnte gezeigt werden, dass 50% der antigen-spezifischen CD8+ T-Zellen nach Aktivierung durch B-Zellen CD40L hochregulieren. Sowohl auf RNA- als auch auf Proteinebene induzierten CD8+CD40L+ T-Zellen einen B-Zell Phänotyp, der stark dem von CD4+ T-Zellen stimulierten B-Zellen ähnelte. In Infektionsversuchen mit dem B-Zell-trophen Virus MHV-68 konnte gezeigt werden, dass transgene Mäuse mit CD40L defizienten CD8+ T-Zellen im Vergleich zu Kontrolltieren eine signifikante Reduktion der Keimzentrums-B-Zellen in den Lymphknoten der oberen Halsregion aufweisen. Eine genauere Betrachtung des B-Zell Repertoires von IgG Gedächtniszellen ergab jedoch, dass die Sequenzen der IGHJ3 Genfamilie bevorzugt für die Modifikation der CDR3 Region in Mäusen mit CD40L defizienten CD8+ T-Zellen verwendet wird, die eine entscheidende Rolle bei der Antigenerkennung spielt. Zusammengefasst kann mit dieser Arbeit zum ersten Mal gezeigt werden, dass CD8+CD40L+ T-Zellen Helferfunktionen durch Unterstützung der B-Zell Aktivierung und Bildung von Keimzentren übernehmen können.
CTLs are important for the elimination of infected and degenerated cells by inducing apoptosis of the target cells. Recently our group identified a sub-population of CD8+ T cells expressing CD40L instead of common CTL markers. To that date, transient CD40L expression on T cells has been only described as a function of activated CD4+ T cells, which displays this key molecule for CD4+ T cell mediated help by binding to the CD40 receptor on other immune cells. Particularly, CD40L signaling provided by CD4+ T cells is indispensable for T cell dependent B cell activation and GC responses, which generate B cells secreting high affinity antibodies that protect the host from invading pathogens. Due to its associated helper functions, this thesis aimed to dissect whether CD40L positive CD8+ T cells are restricted to cytotoxic killing or if this sub-population possesses similar properties as CD4+ T cells when interacting with B cells. In vitro co-culture experiments showed that 50% of murine antigen specific CD8+ T cells up-regulated CD40L upon activation by antigen presenting B cells. When compared to CD40L deficient CD8+ T cells, the interaction of CD8+ CD40L+ T cells induced remarkable changes in B cells on the RNA and protein level and triggered a B cell phenotype resembling that of B cells primed by CD4+ T cells. By the infection of mice with the B cell trophic virus MHV-68, it was found that E8IcrexCD40Lflox transgenic mice lacking CD40L only on matured CD8+ T cells, exhibited a significant decrease of GC B cells in superficial cervical lymph nodes at the acute state of infection compared to WT mice. A closer look into the memory B cell repertoire revealed a preferred usage of the murine IGHJ3 gene family that modifies the CDR3 and thus the recognition groove of the B cell antibody in E8IcrexCD40Lflox mice. In summary, this work provides sufficient evidence that CD8+ CD40L+ T cells adopt helper-like functions by supporting B cell activation and subsequent GC formation.
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Abduh, Maisa. "Follicular CD4 T Cells Tutor CD8 Early Memory Precursors : an Initiatory Journey to the Frontier of B Cell Territory." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS371.

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Les lymphocytes T CD8+ spécifiques de l'antigène sont impliqués dans la réponse immunitaire adaptative et jouent un rôle essentiel dans la protection de l'hôte contre l'infection par des pathogènes intracellulaires. Cette protection de longue durée dépend de la génération de réponses lymphocytaires T CD8+ mémoires, hautement fonctionnelles en termes de fréquence et de fonctionnalité, après réinfection.Après présentation de l'antigène, une cellule T CD8 naïve subit une forte expansion clonale, générant une population hétérogène de cellules activées qui est dominée, au sommet de l'expansion, par des effecteurs CD8 de courte durée (SLEC). Cette expansion est suivie d'une phase de contraction massive par apoptose. Quelques cellules survivent à cette phase de contraction et finissent par se différencier en cellules mémoire hautement compétentes. Les processus par lesquels et le moment où se différencient les précurseurs de mémoire (MPECs) restent largement inconnus, tout comme les étapes ultérieures de leur maturation en cellules mémoire pleinement fonctionnelles. Les signaux d'aide provenant des cellules T CD4+ sont clairement requis tout au long du processus de maturation des MPEC.Notre équipe a montré que les lymphocytes T CD4+ régulateurs FoxP3+ (Tregs) favorisent la maturation des MPEC en limitant l'exposition à l'IL-2 et en fournissant des signaux inhibiteurs, mais ce n'est probablement qu'une facette de l'aide complexe et multiforme apportée par les cellules T CD4+ au MPEC. Les Tregs agissent sur des MPEC préexistants. Les réponses mémoire B et CD8+ partagent des caractéristiques communes, telles que l'expression du facteur de transcription Bcl-6. Les lymphocytes T CD4+ folliculaires (Tfh) sont les principaux producteurs de la cytokine IL-21. Bien que les mécanismes par lesquels les Tfh induisent l’expression de Bcl-6 dans les cellules B doivent être clarifiés, ils pourraient inclure l’IL-21 et l’interaction CD40-CD40L.Dans ce projet de thèse, nous avons étudié le rôle potentiel des Tfh dans l'initiation de la différenciation mémoire T CD8+, dans des modèles de souris transgéniques permettant une déplétion transitoire et sélective des Tfh, infectées par la bactérie recombinante Listeria monocytogenes-OVA.Nous avons montré que dès 2 jours après l'infection, les MPECs très précoces peuvent être identifiés par l’expression du récepteur de chimiokine CXCR5. Ces précurseurs précoces, qui ont un phénotype effecteur, se développent et migrent temporairement à la jonction des zones T et B, où ils interagissent avec les Tfh puis perdent leur expression CXCR5.Cette interaction avec les Tfh, considérés jusqu'à présent comme des auxiliaires exclusifs des cellules B, est nécessaire pour que les MPECs CD8+ deviennent des cellules mémoire compétentes sensibles à l'IL-21, capables de générer des réponses effectrices secondaires efficaces.Cette étude dévoile les premières étapes cruciales dans la génération de la mémoire CD8+, identifie CXCR5 comme le premier marqueur connu des MPECs CD8+, révèle l’implication fondamentale des Tfh dans le CD4 help et indique une coordination possible, via les Tfh, entre les voies de différentiation mémoire CD8+ et B. Ces résultats peuvent avoir des implications pour la conception du vaccin et de l'immunothérapie
Antigen-specific CD8 T cells are involved in the adaptive immune response and play a critical role in protecting the host from infection by intracellular pathogens. This long-lasting protection depends on the generation of memory CD8+ T cell responses, which are highly functional in terms of frequency and functionality, after secondary infection.Following antigen activation, a naive CD8 T cell undergoes strong clonal expansion, generating a heterogeneous population of activated cells that is dominated, at the peak of expansion, by short-lived CD8 effectors (SLECs). This expansion is followed by a phase of drastic contraction through massive apoptosis. A few cells survive this contraction phase and eventually become highly competent memory cells. Precisely when and how these memory precursors (MPECs) are generated is largely unknown, and so are the subsequent steps of their maturation into fully functional memory cells. Help signals from CD4+ T cells are clearly required throughout the MPEC maturation process.Our team has previously shown that FoxP3+ regulatory CD4+ T cells (Tregs) favor MPECs maturation by limiting exposure to IL-2 and by providing inhibitory signals, but this is probably only one facet of the complex and multifaceted help provided by CD4+ T cells to MPEC, and Tregs act on pre-existing MPECs.B-cell memory and CD8+ T cell memory share some common features, such as the expression of the transcription factor Bcl-6. Tfh are major producers of the cytokine IL-21. The mechanisms by which Tfh induces Bcl-6 in B-cells need to be clarified, they might include IL-21 and CD40-CD40L.In this PhD project, we have investigated the potential role of Tfh on the initiation of CD8 memory differentiation, in transgenic mice models, allowing transient and selective depletion of Tfh cells, infected by recombinant Listeria monocytogenes-OVA.We have shown that as early as 2 days after infection, very early memory precursors can be identified by their expression of the chemokine receptor CXCR5. These early precursors, which have an effector phenotype, expand and temporarily migrate to the junction of T-cell and B-cell zones, where they interact with follicular CD4 T cells (Tfh) then lose their CXCR5 expression.Remarkably, this interaction with Tfh, hitherto considered as exclusive B-cell helpers, is required for memory precursors to become competent memory cells responsive to IL-21 and capable of mounting efficient cytotoxic secondary effector responses.This study thus unveils critical early steps in the generation of CD8 memory, identifies CXCR5 as the earliest known marker of CD8 memory precursors, reveals a major helper role for Tfh, and points to possible coordination, through Tfh, between the pathways of CD8 and B-cell memory generation. These findings may have implications for vaccine and immunotherapy design
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3

Loyal, Lucie. "The molecular regulation of CD40L in CD8+ T cells." Doctoral thesis, Humboldt-Universität zu Berlin, 2019. http://dx.doi.org/10.18452/20158.

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T Zellen können in zwei Hauptpopulationen mit unterschiedlichen Aufgaben unterschieden werden. CD4+ T Zellen exprimieren im Zuge ihrer Aktivierung CD40L, welches ein zentraler kostimulatorischer Rezeptor zur Induktion von B-Zell basierter humoraler Immunität, APC Aktivierung und einer effizienten Effektor CD8+ T Zell Entwicklung ist („Helfer-Funktion“). Im Gegensatz dazu sind die zytotoxischen CD8+ T Zellen dazu vorbestimmt, infizierte oder maligne Zellen direkt abzutöten. Jedoch wurde eine Fraktion von CD8+ T Zellen identifiziert, die nach Aktivierung CD40L exprimiert. Bisher ist nicht verstanden, wie in solchen CD8+ T Zellen a) die CD40L Expression reguliert ist, b) wann und wie die Fähigkeit CD40L zu exprimieren implementiert wird und c) was die Folgen für das Immunsystem sind. In dieser Arbeit konnten wir zeigen, dass sowohl in CD4+ als auch in CD8+ T Zellen die CD40L Expression durch DNA-Methylierung regulatorischer Regionen des CD40LG Lokus reguliert wird. Die Demethylierung zentraler Elemente wird im Thymus implementiert, manifestiert sich mit der T-Zell Reifung und geht mit einer zunehmenden Stabilität der CD40L Expression einher. Erhöhte Expression von CD5 und NUR77 in CD40L+ CD8+ SP Thymozyten weisen auf eine positive Selektion mit hoher Affinität gegen Selbst-peptide während der Reifung im Thymus hin, welche das weitere Schicksal der CD40L exprimierenden CD8+ T Zellen beeinflusst. Naive CD40L+ CD8+ T Zellen besitzen ein anderes TCR Repertoire als CD40L- CD8+ T Zellen und reifen im Zuge ihrer Aktivierung bevorzugt zu Gedächtniszellen mit Zytokin- und Chemokinrezeptorprofilen von Tc2, Tc17 und Tc22 Zellen heran. Mit ihrem nicht-zytotoxischen Phänotyp und ihrer Genexpressionsignatur ähneln diese Zellen stark Helfer-CD4+ T Zellen und können von den klassisch zytotoxischen Tc1 und Tc17+1 Zellen durch ihre IL-6R und fehlende SLAMF7 Expression sowie der Expression von Markern die auf eine Fähigkeit in die Haut zu wandern schließen lassen, unterschieden werden. Zusammenfassend zeigen wir hier, dass naive CD8+ T Zellen von den frühsten Entwicklungsstadien im Thymus an nicht homogen sind und die Fähigkeiten über CD40L Expression eine Helferfunktion auszuüben beziehungsweise über die Sekretion zytolytischer Moleküle Zielzellen abzutöten unabhängig vom CD4+ or CD8+ T-Zell Status sind. Zellen mit Zytokin- und Genexpressionsignaturen, die mit denen der CD8+ Helfer-T Zellen übereinstimmen, wurden von uns und anderen in Geweben (Haut, Lunge) identifiziert und tragen zu den verschiedensten autoinflammatorischen Erkrankungen bei. Diese Arbeit insinuiert daher die Notwendigkeit einer grundlegenen Neubewertung der CD8+ T Zell Fähigkeiten und Funktionen in Immunantworten.
The T cell compartment consists of two major subsets with diverse assignments. CD4+ T cells express CD40L upon activation, a central co-stimulatory receptor to induce B cell mediated humoral immunity, activate APCs and prime efficient effector CD8+ T cell development (“helper function”). In contrast, cytotoxic CD8+ T cells are predetermined to kill infected or malignant cells directly. However, a fraction of CD8+ T cells expressing CD40L upon activation was identified. So far, it is not understood in CD8+ T cells a) how CD40L expression is regulated, b) when and how the ability of CD40L expression is implemented and c) what are the implications for the immune system. In this thesis, we found that CD40L expression is regulated by DNA-methylation of regulatory regions of the CD40LG locus in CD4+ as well as CD8+ T cells. The de-methylation of central elements is implemented in the thymus and increases with T cell maturation reflected by enhanced stability of CD40L expression. Elevated CD5 and NUR77 expression of CD40L+ CD8+ SP thymocytes suggests that high affine detection of self-peptides during positive selection in the thymus implements CD40L expression ability and predetermines the fate of the CD40L imprinted CD8+ T cells. CD40L+ naïve CD8+ T cells differ in their TCR repertoire from their CD40L- counterparts and preferentially mature into memory cell subsets with cytokine and chemokine receptor profiles of Tc2, Tc17 and Tc22 cells. With their non-cytotoxic phenotype and gene expression signatures, the CD40L+ memory CD8+ T cell subsets Tc2, Tc17 and Tc22 widely resemble helper CD4+ T cells and can be distinguished from classical cytotoxic Tc1 and Tc17+1 cells by their IL-6R and absent SLAMF7 expression and their skin migratory phenotype. Altogether, we demonstrate that from the earliest developmental stages in thymus onwards naive CD8+ T cells are not homogenous and the abilites to provide “CD40L based help” or “cytotoxicity mediated killing” are independent of the CD4+ or CD8+ T cell status. Cells with helper-type CD8+ T cell cytokine and gene-expression signatures were found at barrier sites (skin, lung) by us and others where they contribute to multiple autoinflammatory diseases. Therefore, this work insinuates the need to revisite CD8+ T cell capablities and function in immune responses.
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Hirano, Ayumi. "T dependent B cell help in cattle : immunoregulatory function of interleukin-4 and CD40-CD40L interactions /." free to MU campus, to others for purchase, 1997. http://wwwlib.umi.com/cr/mo/fullcit?p9841150.

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Schubert, Lisa Ann. "Characterization of the transcriptional regulation of the human CD40L gene in CD4 T cells /." Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/8325.

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Mühle, Kerstin [Verfasser], Hans-Dieter [Gutachter] Volk, Andreas [Gutachter] Thiel, and Ulf [Gutachter] Wagner. "Interaction of CD8+CD40L+ T cells with B cells / Kerstin Mühle ; Gutachter: Hans-Dieter Volk, Andreas Thiel, Ulf Wagner." Berlin : Humboldt-Universität zu Berlin, 2018. http://d-nb.info/1185495924/34.

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Loyal, Lucie [Verfasser], Andreas [Gutachter] Thiel, Chiara [Gutachter] Romagnani, and Hans-Dieter [Gutachter] Volk. "The molecular regulation of CD40L in CD8+ T cells / Lucie Loyal ; Gutachter: Andreas Thiel, Chiara Romagnani, Hans-Dieter Volk." Berlin : Humboldt-Universität zu Berlin, 2019. http://d-nb.info/1190641046/34.

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Harlin, Helena. "TRAF4 and CD30/TRAF2 in normal T cell function /." 2001. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:3019923.

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Chen, Jui-Chieh, and 陳瑞傑. "The inhibition of T cell proliferation by CD30 expression on the Hodgkin’s cancer cell." Thesis, 2003. http://ndltd.ncl.edu.tw/handle/49838763617401022976.

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碩士
國立臺灣大學
生物化學暨分子生物學研究所
91
英文摘要 Hodgkin''s disease is a type of malignant lymphoma, characterized by the presence of abnormal cells, named Reed-Sternberg cells, in patient’s lymph nodes. CD30 was originally described as a marker of Hodgkin/Reed-Sternberg cells. CD30 and its cognate ligand, CD153, belong to members of the TNFR and TNF superfamilies, respectively. CD30 is expressed on the surface of Hodgkin/Reed-Sternberg (H-RS) cell lines (KM-H2), while expression of CD153 can be induced on the surface of peripheral blood T cells by anti-CD3 or PHA activation. In this study, we addressed the effect of CD30 reverse signaling on T cells. By co-cultures of KM-H2 and PBMC activated by anti-CD3 or PHA, we observed T cell proliferation was inhibited. The inhibition was not dependent on cytokines or substances released from KM-H2, because KM-H2 cells were fixed with paraformaldehyde before the co-culture. We further study the effect of CD30 on T cell proliferation with CD30-expressing Chinese Hamster Ovary (CHO) cells to. In the presence of CD30-positive CHO cells, PHA-treated PBMC failed to achieve significant proliferation. Similar effects were observed if PHA-treated PBMC were cultured in the medium containing chimeric CD30-Fc fusion proteins. Taken together, we discover the inhibitory effect of CD30 reverse signaling on CD153-positive T cells. Furthermore, in order to characterize the protein expression profile in response to CD30 reverse signaling, proteomic technology was used. Several candidate spots were found to be likely regulated by CD30 engagement. One of these spots was identified as Mn-SOD by the use of MALDI-TOF MS. We conclude that H-RS cells are able to inhibit the proliferation of activated T cells through the CD30-CD153 interaction, which may lead to a microenvironment in favor of the growth and survival of the tumor cells.
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Boyle, Julia Katrina. "The role of CD30 in the regulation of T cell function." Thesis, 2003. http://hdl.handle.net/2429/14546.

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CD30 is a member of the TNFR superfamily that was initially identified on Reed-Sternberg cells of Hodgkin's disease and is widely expressed in other lymphomas as well as in a number of autoimmune diseases. On normal cells, CD30 is expressed primarily on activated CD8⁺ T cells and is induced by two distinct pathways, an IL-4 dependent pathway and an IL-4-independent pathway via CD28. The precise role of CD30 has been controversial, but it has been implicated in a number of T cell functions, including costimulation, cytokine production, cell survival and cytotoxicity, although much of the published work to date has been carried out in cell lines. In an attempt to elucidate the role of CD30 in normal T cells, the function of primary lymphocytes derived from CD30-deficient mice was studied. In the absence of CD30, proliferation and activation were normal, with CD30[sup -/-] cells exhibiting levels of proliferation and expression of activation markers comparable to that of wild type cells. As well, among those cytokines examined, production by activated CD30-deficient cells was normal, although production of IL-4 was reduced compared to wild type. 2C-transgenic CD30-deficient cells were unable to kill specific target cells to the same extent as wild type effectors, although expression of effector molecules including perforin, granzyme B and FasL was normal, as was killing of targets when the requirement for TCR recognition was bypassed. Finally, although the reduction of effector function suggested that memory development may also be effected, 2C/CD30[sup -/-] effectors were able to develop into memory-like cells to the same extent as wild type cells. Although the deletion of CD30 has little effect on a number of T cell functions, particularly activation and proliferation, it appears that CD30 does play a role in the regulation of later events such as cytotoxic effector function and the maintenance of IL-4 production.
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Books on the topic "CD30L T cell"

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Lucas, Carrie Lynn. Mechanisms of deletional tolerance of peripheral CD8⁺ T cells induced by anti-CD40L and allogeneic bone marrow transplantation. 2010.

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Book chapters on the topic "CD30L T cell"

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Kadin, Marshall E., and Francine Foss. "Primary Cutaneous and Systemic CD30+ T-cell Lymphoproliferative Disorders." In T-Cell Lymphomas, 71–86. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-170-7_5.

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Kaudewitz, Peter, Iannis Anagnostopoulos, Michael Hummel, and Harald Stein. "HTLV-1 Proviral Sequences in Cutaneous CD30-Positive T Large Cell Lymphomas." In Basic Mechanisms of Physiologic and Aberrant Lymphoproliferation in the Skin, 195–204. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-1861-7_14.

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Wood, G. S., J. W. Gould, and A. C. Gilliam. "Primary cutaneous CD30+ large-cell lymphoma with natural killer-cell phenotype and the t(2;5) translocation." In Cutaneous Lymphomas, 40–41. Heidelberg: Steinkopff, 2001. http://dx.doi.org/10.1007/978-3-642-57624-9_20.

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Kazlouskaya, V., J. Ho, and O. E. Akilov. "Case 42. Primary cutaneous CD30 T-cell posttransplant lymphoproliferative disorder with δ expression." In Cutaneous Lymphomas, 98–99. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-59129-8_42.

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"CD30+ cutaneous large T-cell lymphoma." In Dermatology Therapy, 120. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/3-540-29668-9_525.

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"Cd30þ T-cell Lymphoproliferative Disorders Of The Skin." In Cutaneous Lymphomas, 193–210. CRC Press, 2005. http://dx.doi.org/10.1201/9780849346033-33.

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Kadin, Marshall E. "Primary Cutaneous CD30-Positive T-Cell Lymphoproliferative Disorders." In Hematopathology, 604–16. Elsevier, 2011. http://dx.doi.org/10.1016/b978-0-7216-0040-6.00039-3.

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"Cd30-Positive Lymphoproliferative Disorders Including Lymphomatoid Papulosis, Borderline Cd30-Positive Lymphoproliferative Disease, Anaplastic Large Cell Lymphoma, and T-Cell-Rich Cd30-Positive Large B Cell Lymphoma." In The Cutaneous Lymphoid Proliferations, 274–311. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781118776193.ch13.

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Conference papers on the topic "CD30L T cell"

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Rana, Seema, and Rajiv Tangri. "Anaplastic large cell lymphoma ALK negative vs. peripheral T cell lymphoma (NOS) - diagnostic dilemma." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685354.

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Middle aged female presented with generalised lymphadenopathy and fever for last one month. Peripheral blood findings were within normal limits. There was no extra nodal involvement. FNAC performed initially from a cervical node suggested possibility of Hodgkin’s lymphoma and a whole node biopsy was performed. Histopathogical examination revealed effaced nodal architecture and a polymorphous population of lymphocytes, plasma cells, neutrophils and scattered large mononuclear cells with prominent nucleolus. An initial panel of CD3, CD20, LCA, CD15, CD30 and PAX5 was performed. The large atypical cells were positive for LCA, CD3 and CD30 with variable positivity for CD15. CD 30 showed Golgi and membranous staining. These large atypical cells were negative for PAX5 and CD20. In view of above findings, Hodgkin’s lymphoma was ruled out and a possibility of Non- Hodgkin’s lymphoma was considered. Further IHC markers were performed which included CD2, CD5, CD7, EMA, Alk, CD10 and KI67. CD5 showed variable positivity. The cells of interest were negative for CD2, CD7, ALK and EMA. Ki 67 index was 70-80%. Overall histological and IHC findings favoured Alk negative Anaplastic large cell lymphoma. Differential diagnosis considered was peripheral T cell lymphoma (NOS). Hodgkin’s lymphoma, peripheral T cell lymphoma (NOS) and anaplastic large cell lymphoma share common histomorphological findings. With careful analysis of Immunohistochemistry, it is easier to categorise Hodgkin’s lymphoma. ALK negative anaplastic large cell lymphoma and peripheral T cell lymphoma (NOS) are difficult to categorise and show overlapping features. We in this case have discussed clinical, histomorphological and IHC pattern of Alk negative Anaplastic large cell lymphoma.
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Heiser, Ryan A., Bryan M. Grogan, Luke S. Manlove, and Shyra J. Gardai. "Abstract 1789: CD30+T regulatory cells, but not CD30+CD8 T cells, are impaired following brentuximab vedotin treatment in vitro and in vivo." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1789.

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Wu, Yang, Dan Chen, Rong Ma, Jun-ying Zhang, Yuan Zhang, Hai-xia Cao, Zhuo Wang, et al. "Abstract 1444: The new therapy strategy for treatment of peripheral T cell lymphomas: CD30-targeted CAR-modified T cell therapy." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1444.

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Wu, Yang, Dan Chen, Rong Ma, Jun-ying Zhang, Yuan Zhang, Hai-xia Cao, Zhuo Wang, et al. "Abstract 1444: The new therapy strategy for treatment of peripheral T cell lymphomas: CD30-targeted CAR-modified T cell therapy." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1444.

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Escribà-Garcia, Laura, Carmen Alvarez-Fernández, Ana Carolina Caballero, Rydzek Julian, Einsele Hermann, Jorge Sierra, Michael Hudecek, and Javier Briones. "Abstract A028: Memory stem T-cells expressing an optimized CD30-specific chimeric antigen receptor (CAR) efficiently eradicate peripheral T-cell lymphoma in vivo." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-a028.

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Caires, Elisana Maria Santos, Régis Resende Paulinelli, Miliana Tostes Lucatto, Eneida Ribeiro Marinho, and Henrique Moura de Paula. "BREAST IMPLANT–ASSOCIATED ANAPLASTIC LARGE CELL LYMPHOMA (BIA-ALCL): A CASE REPORT WITH ATYPICAL SYMPTOMS." In Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2096.

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The BIA-ALCL is a rare type of T-cell lymphoma CD30+ e AKL−, occurring more common in women with Allergantextured implants. It presents most frequently as a late-onset accumulation of seroma fluid between the implant and less frequently as a palpable tumor mass, with malignant cells infiltrating through the capsule and surrounding tissue with potential lymph node and systemic involvement. This article describes a case report of a 65-year-old female patient with BIA-ALCL complaining of erythema in her right breast for almost 7 months. She agreed no family history of cancer and no fever. The patient was diabetic type 2, dyslipidemic, and postmenopausal taking estrogen therapy. She had undergone a breast augmentation with 215 mL polyurethane-coated implants 15 years ago. Imaging revealed right axillary lymph node enlargement, thickening of the breast parenchyma, and minimal periprosthetic seroma. The initial suspicion was infection wherefore she was submitted removal of the implants, partial capsulectomy on the right side, and total contralateral capsulectomy. Immunochemistry confirmed BIA-ALCL CD30+ e AKL− on the right and no disease on the left. Bacterioscopy was negative. A complementary surgical procedure involving removal of all the right capsules, resection of axillary palpable nodes, and reconstruction was necessary to achieve a bilateral oncoplastic mastopexy. The final diagnosis was BIA-ALCL confined capsule with negative margins and none axillary lymph nodes involvement, staging IB. No adjuvant treatment was necessary. The patient remained symptom free during follow-up examinations, and she desires a new breast augmentation.
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Trella, Emanuele, Evangelos Panoupolos, Swantje Heidtmann, Nermin Raafat, Giulio Cesare Spagnoli, and Paul Zajac. "Abstract 2883: Improved generation of central memory CD8+ T cells with CD40L expressing recombinant vaccinia virus." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2883.

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Merz, Christian, Jaromir Sykora, Viola Marschall, David M. Richards, Meinolf Thiemann, Harald Fricke, Oliver Hill, and Christian Gieffers. "Abstract 1760: The hexavalent CD40 agonist HERA-CD40L augments multi-level crosstalk between T cells and antigen-presenting cells." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1760.

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Kua, Lindsay, Chee Hoe Ng, Jin Wei Tan, Richard Ong, Cheah Chen Seh, Fiona Wong, Don Sim, Ivan David Horak, Lionel Low, and Kar Wai Tan. "240 Humanized CD30 chimeric antigen receptor T cells with a novel 4–1BB derived spacer have improved activity and safety against CD30-positive lymphomas." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0240.

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Cho, Hyun-Il, Chung-Hyo Kang, Sang-Eun Lee, In-Sil Song, Jung-Min Ha, Hyun-Jung Sohn, and Tai-Gyu Kim. "250 Chimeric antigen receptors containing CD30-derived costimulatory domain elicit augmented T cell effector functions and anti-tumor efficacy." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0250.

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