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Journal articles on the topic 'CD27-ligand'

Author: Grafiati

Published: 4 June 2021

Last updated: 13 February 2022

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1

Gravestein, L. A., W. van Ewijk, F. Ossendorp, and J. Borst. "CD27 cooperates with the pre-T cell receptor in the regulation of murine T cell development." Journal of Experimental Medicine 184, no. 2 (1996): 675–85. http://dx.doi.org/10.1084/jem.184.2.675.

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CD27 is a lymphocyte-specific member of the TNF receptor family and has a TNF-related transmembrane ligand, CD70. The CD27/CD70 receptor-ligand pair cooperates with the TCR in the regulation of the peripheral T cell response. The study presented here reveals that CD27 may play a similar role in thymic pre-T cell development. We have previously cloned the cDNA encoding murine CD27, prepared specific mAbs and observed that murine CD27 is expressed on virtually all thymocytes, with the exception of a subpopulation of CD4-8- precursor T cells. It is shown here that induction of murine CD27 express

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2

Hintzen, Rogier Q., Susanne M. A. Lens, Gerrit Koopman, Steven T. Pals, Hergen Spits, and René A. W. van Lier. "CD70 represents the human ligand for CD27." International Immunology 6, no. 3 (1994): 477–80. http://dx.doi.org/10.1093/intimm/6.3.477.

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3

Ranheim, EA, MJ Cantwell, and TJ Kipps. "Expression of CD27 and its ligand, CD70, on chronic lymphocytic leukemia B cells." Blood 85, no. 12 (1995): 3556–65. http://dx.doi.org/10.1182/blood.v85.12.3556.bloodjournal85123556.

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Crosslinking the CD27 antigen on T cells provides a costimulatory signal that, in concert with T-cell receptor crosslinking, can induce T-cell proliferation and cellular immune activation. We find that chronic lymphocytic leukemia (CLL) B cells from most patients coexpress both membrane-bound and soluble CD27, along with its newly identified ligand, CD70. The expression of soluble CD27 may preclude leukemic B cells from stimulating T cells via CD70, thereby potentially impairing their ability to function as effective antigen-presenting cells. We find that leukemic B-cell expression of soluble

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4

Teplyakov, Alexey, Galina Obmolova, Thomas J. Malia, and Gary L. Gilliland. "Crystal structure of CD27 in complex with a neutralizing noncompeting antibody." Acta Crystallographica Section F Structural Biology Communications 73, no. 5 (2017): 294–99. http://dx.doi.org/10.1107/s2053230x17005957.

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CD27 is a T-cell and B-cell co-stimulatory glycoprotein of the tumor necrosis factor (TNF) receptor superfamily that is dependent on the availability of the TNF-like ligand CD70. Therapeutic approaches to treating autoimmune diseases and cancers with antagonistic and agonistic anti-CD27 monoclonal antibodies (mAbs), respectively, have recently been developed. Mouse anti-human CD27 mAb 2177 shows potency in neutralizing CD70-induced signaling; however, it does not block the binding of soluble CD70. To provide insight into the mechanism of action of the mAb, the crystal structure of the CD27 ext

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5

Agematsu, Kazunaga, Haruo Nagumo, Yumiko Oguchi, et al. "Generation of Plasma Cells From Peripheral Blood Memory B Cells: Synergistic Effect of Interleukin-10 and CD27/CD70 Interaction." Blood 91, no. 1 (1998): 173–80. http://dx.doi.org/10.1182/blood.v91.1.173.

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Abstract B cells can differentiate into the antibody-secreting cells, plasma cells, whereas the crucial signals that positively control the entry into the pathway to plasma cells have been unclear. Triggering via CD27 by CD27 ligand (CD70) on purified peripheral blood B cells yielded an increase in the number of plasma cells in the presence of interleukin-10 (IL-10). Differentiation into plasma cells by a combination of IL-10 and CD70 transfectants occurred in CD27+ B cells but not in CD27− B cells. Moreover, addition of IL-2 to the IL-10 and CD70-transfect activation system greatly induced di

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6

Agematsu, Kazunaga, Haruo Nagumo, Yumiko Oguchi, et al. "Generation of Plasma Cells From Peripheral Blood Memory B Cells: Synergistic Effect of Interleukin-10 and CD27/CD70 Interaction." Blood 91, no. 1 (1998): 173–80. http://dx.doi.org/10.1182/blood.v91.1.173.173_173_180.

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B cells can differentiate into the antibody-secreting cells, plasma cells, whereas the crucial signals that positively control the entry into the pathway to plasma cells have been unclear. Triggering via CD27 by CD27 ligand (CD70) on purified peripheral blood B cells yielded an increase in the number of plasma cells in the presence of interleukin-10 (IL-10). Differentiation into plasma cells by a combination of IL-10 and CD70 transfectants occurred in CD27+ B cells but not in CD27− B cells. Moreover, addition of IL-2 to the IL-10 and CD70-transfect activation system greatly induced differentia

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7

Ochsenbein, Adrian F., Stanley R. Riddell, Michele Brown, et al. "CD27 Expression Promotes Long-Term Survival of Functional Effector–Memory CD8+Cytotoxic T Lymphocytes in HIV-infected Patients." Journal of Experimental Medicine 200, no. 11 (2004): 1407–17. http://dx.doi.org/10.1084/jem.20040717.

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Human immunodeficiency virus (HIV)-specific CD8+ T cells persist in high frequencies in HIV-infected patients despite impaired CD4+ T helper response to the virus, but, unlike other differentiated effector cytotoxic T lymphocytes, most continue to express the tumor necrosis factor receptor family member CD27. Because the ligand for CD27 (CD70) is also overexpressed in HIV-infected hosts, we examined the nature of expression and potential functional consequences of CD27 expression on HIV-specific CD8+ T cells. Analysis of CD27+ and CD27− T cells derived from the same HIV-specific clone revealed

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8

Tai, Yu-Tzu, Xian-Feng Li, Rory Coffey, et al. "CD27-Mediated Apoptosis Is Dependent on Siva-Induced Caspase Activation in Human Multiple Myeloma." Blood 106, no. 11 (2005): 3398. http://dx.doi.org/10.1182/blood.v106.11.3398.3398.

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Abstract CD27, a member of tumor necrosis factor receptor superfamily that lacks a death domain in its cytoplasmic region, and its interaction with its ligand, CD70, is crucial for differentiation into plasma cells. In malignant B cells, aberrant expression and reverse signaling of CD70 might contribute to disease progression. Recent studies showed that CD27 is heterogeneously expressed on multiple myeloma (MM) plasma cells and the expression is reduced with the progression of MM. However, a possible role for the loss of CD27-CD70 interaction in myelomagenesis was never defined. In this study,

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9

Deng, Yun, Bithi Chatterjee, Kyra Zens, et al. "CD27 is required for protective lytic EBV antigen–specific CD8+ T-cell expansion." Blood 137, no. 23 (2021): 3225–36. http://dx.doi.org/10.1182/blood.2020009482.

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Abstract Primary immunodeficiencies in the costimulatory molecule CD27 and its ligand, CD70, predispose for pathologies of uncontrolled Epstein-Barr virus (EBV) infection in nearly all affected patients. We demonstrate that both depletion of CD27+ cells and antibody blocking of CD27 interaction with CD70 cause uncontrolled EBV infection in mice with reconstituted human immune system components. While overall CD8+ T-cell expansion and composition are unaltered after antibody blocking of CD27, only some EBV-specific CD8+ T-cell responses, exemplified by early lytic EBV antigen BMLF1-specific CD8

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10

Riether, Carsten, Christian M. Schürch, Elias D. Bührer, et al. "CD70/CD27 signaling promotes blast stemness and is a viable therapeutic target in acute myeloid leukemia." Journal of Experimental Medicine 214, no. 2 (2016): 359–80. http://dx.doi.org/10.1084/jem.20152008.

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Aberrant proliferation, symmetric self-renewal, increased survival, and defective differentiation of malignant blasts are key oncogenic drivers in acute myeloid leukemia (AML). Stem cell gene signatures predict poor prognosis in AML patients; however, with few exceptions, these deregulated molecular pathways cannot be targeted therapeutically. In this study, we demonstrate that the TNF superfamily ligand–receptor pair CD70/CD27 is expressed on AML blasts and AML stem/progenitor cells. CD70/CD27 signaling in AML cells activates stem cell gene expression programs, including the Wnt pathway, and

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11

Starzer, Angelika M., and Anna S. Berghoff. "New emerging targets in cancer immunotherapy: CD27 (TNFRSF7)." ESMO Open 4, Suppl 3 (2020): e000629. http://dx.doi.org/10.1136/esmoopen-2019-000629.

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Cluster of differentiation 27 (CD27) is a member of the tumour necrosis factor receptor superfamily and plays a key role in T-cell activation by providing a costimulatory signal. Bound to its natural ligand CD70, CD27 signalling enhances T-cell proliferation and differentiation to effector and memory T cells and therefore has potential as an immune modulatory target in cancer treatment. The CD27 agonistic antibody varlilumab showed promising efficacy in haematological as well as solid cancers. Current studies investigate the combination of the CD27 agonistic antibody varlilumab in combination

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12

Izawa, Kazushi, Emmanuel Martin, Claire Soudais, et al. "Inherited CD70 deficiency in humans reveals a critical role for the CD70–CD27 pathway in immunity to Epstein-Barr virus infection." Journal of Experimental Medicine 214, no. 1 (2016): 73–89. http://dx.doi.org/10.1084/jem.20160784.

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Epstein-Barr virus (EBV) infection in humans is a major trigger of malignant and nonmalignant B cell proliferations. CD27 is a co-stimulatory molecule of T cells, and inherited CD27 deficiency is characterized by high susceptibility to EBV infection, though the underlying pathological mechanisms have not yet been identified. In this study, we report a patient suffering from recurrent EBV-induced B cell proliferations including Hodgkin’s lymphoma because of a deficiency in CD70, the ligand of CD27. We show that EBV-specific T lymphocytes did not expand properly when stimulated with CD70-deficie

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13

Coquet, Jonathan M., Julie C. Ribot, Nikolina Bąbała, et al. "Epithelial and dendritic cells in the thymic medulla promote CD4+Foxp3+ regulatory T cell development via the CD27–CD70 pathway." Journal of Experimental Medicine 210, no. 4 (2013): 715–28. http://dx.doi.org/10.1084/jem.20112061.

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CD4+Foxp3+ regulatory T cells (Treg cells) are largely autoreactive yet escape clonal deletion in the thymus. We demonstrate here that CD27–CD70 co-stimulation in the thymus rescues developing Treg cells from apoptosis and thereby promotes Treg cell generation. Genetic ablation of CD27 or its ligand CD70 reduced Treg cell numbers in the thymus and peripheral lymphoid organs, whereas it did not alter conventional CD4+Foxp3− T cell numbers. The CD27–CD70 pathway was not required for pre-Treg cell generation, Foxp3 induction, or mature Treg cell function. Rather, CD27 signaling enhanced positive

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14

Ho, Allen W., Xavier Leleu, Evdoxia Hatjiharissi, et al. "A Novel Functional Role for Soluble CD27 in the Pathogenesis of Waldenstrom’s Macroglobulinemia." Blood 106, no. 11 (2005): 4701. http://dx.doi.org/10.1182/blood.v106.11.4701.4701.

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Abstract The tumor necrosis factor (TNF) receptor family member, CD27, is a transmembrane co-stimulatory molecule present on primed T and B lymphocytes that also secrete a soluble form (sCD27). Recent evidence has suggested that interactions between CD27 and its TNF-like ligand, CD70, play a critical role in regulating B-cell activation and survival, though the detailed mechanism(s) by which this occurs remain unclear. Waldenstrom’s Macroglobulinemia (WM) represents a lymphoplasmacytic lymphoma characterized by a monoclonal IgM gammopathy and possesses a mast cell component that may contribute

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15

Lens, Susanne M. A., Rolien De Jong, Berend Hooibrink, et al. "Phenotype and function of human B cells expressing CD70 (CD27 ligand)." European Journal of Immunology 26, no. 12 (1996): 2964–71. http://dx.doi.org/10.1002/eji.1830261223.

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16

Ho, A. W., E. Hatjiharissi, A. Branagan, et al. "Therapeutic targeting of CD70 and CD27-CD70 interactions with the monoclonal antibody SGN-70 in Waldenstrom’s Macroglobulinemia (WM)." Journal of Clinical Oncology 24, no. 18_suppl (2006): 2509. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.2509.

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2509 Background: WM represents a lymphoplasmacytic lymphoma characterized by a monoclonal IgM gammopathy and possesses a mast cell component that may contribute to its pathogenesis. The tumor necrosis factor (TNF) receptor family member, CD27, is a transmembrane co-stimulatory molecule that is also secreted in a soluble form (sCD27). Recent evidence has suggested that interactions between CD27 and its TNF-like ligand, CD70, play a critical role in regulating B-cell activation and survival, and therefore, may provide a viable therapeutic target for the treatment of WM. Methods: Patients with th

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17

Ghosh, Sujal, Sevgi Köstel Bal, Emily S. J. Edwards, et al. "Extended clinical and immunological phenotype and transplant outcome in CD27 and CD70 deficiency." Blood 136, no. 23 (2020): 2638–55. http://dx.doi.org/10.1182/blood.2020006738.

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Abstract Biallelic mutations in the genes encoding CD27 or its ligand CD70 underlie inborn errors of immunity (IEIs) characterized predominantly by Epstein-Barr virus (EBV)-associated immune dysregulation, such as chronic viremia, severe infectious mononucleosis, hemophagocytic lymphohistiocytosis (HLH), lymphoproliferation, and malignancy. A comprehensive understanding of the natural history, immune characteristics, and transplant outcomes has remained elusive. Here, in a multi-institutional global collaboration, we collected the clinical information of 49 patients from 29 families (CD27, n =

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18

Descatoire, Marc, Sandra Weller, Sabine Irtan, et al. "Identification of a human splenic marginal zone B cell precursor with NOTCH2-dependent differentiation properties." Journal of Experimental Medicine 211, no. 5 (2014): 987–1000. http://dx.doi.org/10.1084/jem.20132203.

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Mouse splenic marginal zone precursors (MZPs) differentiate into marginal zone B (MZB) cells under a signaling pathway involving Notch2 and its ligand, delta-like 1 ligand (Dll1). We report the identification of an MZP subset in the spleen of young children. These MZPs differentiate into MZ-like B cells in vitro in the presence of OP9 cells expressing human DLL1, as demonstrated by the up-regulation of classical MZB cell markers. A set of diagnostic genes discriminating IgM+IgD+CD27+ blood and splenic MZB cells from switched B cells was identified (up-regulation of SOX7, down-regulation of TOX

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19

Tesselaar, Kiki, Yanling Xiao, Ramon Arens, et al. "Expression of the Murine CD27 Ligand CD70 In Vitro and In Vivo." Journal of Immunology 170, no. 1 (2003): 33–40. http://dx.doi.org/10.4049/jimmunol.170.1.33.

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20

Troeger, Anja, Ludmila Glouchkova, Birgit Ackermann, et al. "Increased TNF/NGF Receptor Expression on BCP-ALL Blasts Carrying the Prognostically Favorable TEL-AML Rearrangement." Blood 110, no. 11 (2007): 1431. http://dx.doi.org/10.1182/blood.v110.11.1431.1431.

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Abstract TEL-AML the most common genetic alteration in childhood precursor B (BCP)-ALL is associated with a favorable prognosis yet the underlying mechanism remains largely unknown. Among the tumor necrosis factor (TNF) receptors CD40 is a key regulator of B cell maturation while nerve growth factor receptor (NGFR), CD27 and CD95 have been implicated in cell cycle arrest and blast apoptosis. Here we prospectively assessed baseline surface expression of the different TNF receptors and the costimulatory molecules CD70, CD80 and CD86 on primary BCP-ALL blasts in a pediatric cohort of TEL-AML posi

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21

Shaw, Joanne, Yui-Hsi Wang, Tomoki Ito, Kazuhiko Arima, and Yong-Jun Liu. "Plasmacytoid dendritic cells regulate B-cell growth and differentiation via CD70." Blood 115, no. 15 (2010): 3051–57. http://dx.doi.org/10.1182/blood-2009-08-239145.

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Abstract The ability of plasmacytoid dendritic cells (pDCs) to promote plasma cell differentiation and immunoglobulin (Ig) secretion through the production of type I interferon and interleukin-6 has been well documented, although the role of additional factors, including tumor necrosis factor receptor-ligand interactions, has not been addressed. On stimulation with the Toll-like receptor ligand CpG (B type, 2006) we found that pDCs exhibit strong and stable expression of CD70, a tumor necrosis factor family ligand that binds to its receptor CD27 expressed on memory B cells and promotes plasma

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22

Ho, Allen W., Evdoxia Hatjiharissi, Bryan T. Ciccarelli, et al. "CD27-CD70 interactions in the pathogenesis of Waldenström macroglobulinemia." Blood 112, no. 12 (2008): 4683–89. http://dx.doi.org/10.1182/blood-2007-04-084525.

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AbstractWaldenström macroglobulinemia (WM) is a B-cell malignancy characterized by an IgM monoclonal gammopathy and bone marrow (BM) infiltration with lymphoplasmacytic cells (LPCs). Excess mast cells (MCs) are commonly present in WM, and provide growth and survival signals to LPCs through several TNF family ligands (CD40L, a proliferation-inducing ligand [APRIL], and B-lymphocyte stimulator factor [BLYS]). As part of these studies, we demonstrated that WM LPCs secrete soluble CD27 (sCD27), which is elevated in patients with WM (P < .001 vs healthy donors), and serves as a faithful marker o

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23

Buchan, Sarah L., Anne Rogel, and Aymen Al-Shamkhani. "The immunobiology of CD27 and OX40 and their potential as targets for cancer immunotherapy." Blood 131, no. 1 (2018): 39–48. http://dx.doi.org/10.1182/blood-2017-07-741025.

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In recent years, monoclonal antibodies (mAbs) able to reinvigorate antitumor T-cell immunity have heralded a paradigm shift in cancer treatment. The most high profile of these mAbs block the inhibitory checkpoint receptors PD-1 and CTLA-4 and have improved life expectancy for patients across a range of tumor types. However, it is becoming increasingly clear that failure of some patients to respond to checkpoint inhibition is attributable to inadequate T-cell priming. For full T-cell activation, 2 signals must be received, and ligands providing the second of these signals, termed costimulation,

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Henson, Sian M., Ornella Franzese, Richard Macaulay, et al. "KLRG1 signaling induces defective Akt (ser473) phosphorylation and proliferative dysfunction of highly differentiated CD8+ T cells." Blood 113, no. 26 (2009): 6619–28. http://dx.doi.org/10.1182/blood-2009-01-199588.

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Abstract Highly differentiated CD8+CD28−CD27− T cells have short telomeres, defective telomerase activity, and reduced capacity for proliferation, indicating that they are close to replicative senescence. In addition, these cells express increased levels of the senescence-associated inhibitory receptor KLRG1 and have poor capacity for IL-2 synthesis and defective Akt (ser473) phosphorylation after activation. It is not known whether signaling via KLRG1 contributes to any of the attenuated differentiation-related functional changes in CD8+ T cells. To address this, we blocked KLRG1 signaling du

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25

Ansell, Stephen M., Ian Flinn, Matthew H. Taylor, et al. "Safety and activity of varlilumab, a novel and first-in-class agonist anti-CD27 antibody, for hematologic malignancies." Blood Advances 4, no. 9 (2020): 1917–26. http://dx.doi.org/10.1182/bloodadvances.2019001079.

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Abstract CD27, a costimulatory molecule on T cells, induces intracellular signals mediating cellular activation, proliferation, effector function, and cell survival on binding to its ligand, CD70. Varlilumab, a novel, first-in-class, agonist immunoglobulin G1 anti-CD27 antibody, mediates antitumor immunity and direct killing of CD27+ tumor cells in animal models. This first-in-human, dose-escalation, and expansion study evaluated varlilumab in patients with hematologic malignancies. Primary objectives were to assess safety and the maximum tolerated and optimal biologic doses of varlilumab. Sec

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Nolte, Martijn A., and René A. W. van Lier. "The price of the CD27–CD70 costimulatory axis: you can't have it all." Journal of Experimental Medicine 203, no. 11 (2006): 2405–8. http://dx.doi.org/10.1084/jem.20061840.

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T cells require costimulatory signals for optimal proliferation, differentiation, and survival and thus to induce protective immune responses. Recent data, however, show that during chronic lymphocyte choriomeningitis virus (LCMV) infection, triggering of the costimulatory receptor CD27 by its ligand CD70 impedes neutralizing antibody production and leads to viral persistence. Thus, while being crucial for the induction of some adaptive effector pathways, costimulation may block the development of others. Pathogens may exploit this Achilles' heal to achieve persistence.

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27

He, Li-Zhen, Larry Thomas, Jeffery Weidlick, et al. "Development of a Human Anti-CD27 Antibody with Efficacy in Lymphoma and Leukemia Models by Two Distinct Mechanisms." Blood 118, no. 21 (2011): 2861. http://dx.doi.org/10.1182/blood.v118.21.2861.2861.

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Abstract Abstract 2861 CD27, a lymphoid cell-specific TNFR superfamily member, is constitutively expressed on the majority of T cells, some NK cells and memory B cells. Through interaction with its ligand CD70, CD27 transduces a co-stimulatory signal promoting T cell and NK cell activation and cytotoxicity. In addition, CD27 is also expressed on many lymphoid-originated hematological neoplastic cells, such as chronic lymphocytic leukemia, mantle cell lymphoma, and Waldenstrom macroglobulinemia, thus being a potential direct target for antibody therapy. To generate potential antibodies for clin

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28

Keller, Anna M., Yanling Xiao, Victor Peperzak, Shalin H. Naik, and Jannie Borst. "Costimulatory ligand CD70 allows induction of CD8+ T-cell immunity by immature dendritic cells in a vaccination setting." Blood 113, no. 21 (2009): 5167–75. http://dx.doi.org/10.1182/blood-2008-03-148007.

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Abstract The use of dendritic cells (DCs) as anticancer vaccines holds promise for therapy but requires optimization. We have explored the potential of costimulatory ligand CD70 to boost the capacity of DCs to evoke effective CD8+ T-cell immunity. We show that immature conventional DCs, when endowed with CD70 expression by transgenesis, are converted from a tolerogenic state into an immunogenic state. Adoptively transferred CD70-expressing immature DCs could prime CD8+ T cells, by CD27, to become tumor-eradicating cytolytic effectors and memory cells with a capacity for robust secondary expans

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Burris, Howard A., Jeffrey R. Infante, Stephen M. Ansell, et al. "Safety and Activity of Varlilumab, a Novel and First-in-Class Agonist Anti-CD27 Antibody, in Patients With Advanced Solid Tumors." Journal of Clinical Oncology 35, no. 18 (2017): 2028–36. http://dx.doi.org/10.1200/jco.2016.70.1508.

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Purpose CD27, a costimulatory molecule on T cells, induces intracellular signals that mediate cellular activation, proliferation, effector function, and cell survival upon binding to its ligand, CD70. Varlilumab is a novel, first-in-class, agonist CD27 antibody that stimulates the CD27 pathway, which results in T-cell activation and antitumor activity in tumor models. This first-in-human, dose-escalation and expansion study evaluated the safety, pharmacology, and activity of varlilumab in patients with advanced solid tumors. Methods In a 3 + 3 dose-escalation design (n = 25), patients received

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30

Padanilam, Babu J., Andrew J. P. Lewington, and Marc R. Hammerman. "Expression of CD27 and ischemia/reperfusion-induced expression of its ligand Siva in rat kidneys." Kidney International 54, no. 6 (1998): 1967–75. http://dx.doi.org/10.1046/j.1523-1755.1998.00197.x.

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Held-Feindt, Janka, and Rolf Mentlein. "CD70/CD27 ligand, a member of the TNF family, is expressed in human brain tumors." International Journal of Cancer 98, no. 3 (2002): 352–56. http://dx.doi.org/10.1002/ijc.10207.

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32

Hamann, Dörte, Paul A. Baars, Martin H. G. Rep, et al. "Phenotypic and Functional Separation of Memory and Effector Human CD8+ T Cells." Journal of Experimental Medicine 186, no. 9 (1997): 1407–18. http://dx.doi.org/10.1084/jem.186.9.1407.

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Human CD8+ memory- and effector-type T cells are poorly defined. We show here that, next to a naive compartment, two discrete primed subpopulations can be found within the circulating human CD8+ T cell subset. First, CD45RA−CD45R0+ cells are reminiscent of memory-type T cells in that they express elevated levels of CD95 (Fas) and the integrin family members CD11a, CD18, CD29, CD49d, and CD49e, compared to naive CD8+ T cells, and are able to secrete not only interleukin (IL) 2 but also interferon γ, tumor necrosis factor α, and IL-4. This subset does not exert cytolytic activity without prior i

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Chaganti, Sridhar, Noelia Begue Pastor, Gouri Baldwin, et al. "EBV Can Induce Somatic Hypermutation in Naïve B Cells In Vitro but Ig Class Switching Requires T Cell Help." Blood 108, no. 11 (2006): 2370. http://dx.doi.org/10.1182/blood.v108.11.2370.2370.

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Abstract Following primary infection, Epstein-Barr virus (EBV) establishes life long persistence in the host IgD− CD27+ memory B cell compartment rather than the IgD+ CD27+ marginal zone (MZ)-like or the IgD+ CD27− naïve B cell compartments. One possible explanation for such exclusive persistence in memory B cells is that EBV preferentially infects memory B cells. Alternatively, the virus may infect all B cell subsets but then drive MZ and naïve B cells to acquire the Ig isotype-switched phenotype and hypermutated Ig genotype of memory cells. Here we ask whether there is any evidence for one

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34

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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35

Erdő-Bonyár, Szabina, Judit Rapp, Tünde Minier, et al. "Toll-Like Receptor Mediated Activation of Natural Autoantibody Producing B Cell Subpopulations in an Autoimmune Disease Model." International Journal of Molecular Sciences 20, no. 24 (2019): 6152. http://dx.doi.org/10.3390/ijms20246152.

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Altered expression and function of the Toll-like receptor (TLR) homologue CD180 molecule in B cells have been associated with autoimmune disorders. In this study, we report decreased expression of CD180 at protein and mRNA levels in peripheral blood B cells of diffuse cutaneous systemic sclerosis (dcSSc) patients. To analyze the effect of CD180 stimulation, together with CpG (TLR9 ligand) treatment, on the phenotype defined by CD19/CD27/IgD/CD24/CD38 staining, and function (CD69 and CD180 expression, cytokine and antibody secretion) of B cell subpopulations, we used tonsillar B cells. After st

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Rojas, José Manuel, Alí Alejo, Jose Miguel Avia, et al. "Activation of OX40 and CD27 Costimulatory Signalling in Sheep through Recombinant Ovine Ligands." Vaccines 8, no. 2 (2020): 333. http://dx.doi.org/10.3390/vaccines8020333.

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Members of the tumour necrosis factor (TNF) superfamily OX40L and CD70 and their receptors are costimulating signalling axes critical for adequate T cell activation in humans and mice but characterisation of these molecules in other species including ruminants is lacking. Here we cloned and expressed the predicted ovine orthologues of the receptors OX40 and CD27, as well as soluble recombinant forms of their potential ovine ligands, OaOX40L and OaCD70. Using biochemical and immunofluorescence analyses, we show that both signalling axes are functional in sheep. We show that oligomeric recombina

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Zambello, Renato, Livio Trentin, Monica Facco, et al. "Analysis of TNF-receptor and ligand superfamily molecules in patients with lymphoproliferative disease of granular lymphocytes." Blood 96, no. 2 (2000): 647–54. http://dx.doi.org/10.1182/blood.v96.2.647.014k18_647_654.

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In 21 patients with lymphoproliferative disease of granular lymphocytes (LDGL), we investigated the expression and the function of molecules belonging to TNF-receptor and TNF-ligand superfamilies (CD30/CD30L; CD40/CD40L; CD27/CD70; Fas [CD95]/FasL[CD95L]). Fourteen patients were characterized by a proliferation of granular lymphocytes (GLs) expressing the CD3+CD16+phenotype, whereas 7 cases showed the CD3−CD16+ CD56 ± phenotype. Our data show that both CD3+ and CD3-GLs are preferentially equipped with CD30, CD40, CD40L, CD70, and CD95 antigens; this pattern is usually associated with the lack

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Sarvaria, Anushruti, Ahmad Khoder, Abdullah Alsuliman, et al. "B Cell With Regulatory Function Are Enriched Within Transitional and IgM Memory B Cell Subsets In Healthy Donors But Are Reduced and Functionally Impaired In Patients With Chronic Graft-Versus-Host Disease." Blood 122, no. 21 (2013): 4478. http://dx.doi.org/10.1182/blood.v122.21.4478.4478.

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The immunosuppressive function of IL10 producing regulatory B cells (Bregs) has been shown in several murine models of inflammation and autoimmune disease. However, there is a paucity of data regarding the existence of an equivalent regulatory B cell subset in healthy individuals and their potential role in the pathogenesis of chronic graft-versus-host disease (cGVHD) remains unknown. Here, we examined the functional regulatory properties of peripheral blood (PB)-derived human B cell subsets from healthy individuals. In addition, we carried out studies to explore their role in cGVHD, using B c

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Zambello, Renato, Livio Trentin, Monica Facco, et al. "Analysis of TNF-receptor and ligand superfamily molecules in patients with lymphoproliferative disease of granular lymphocytes." Blood 96, no. 2 (2000): 647–54. http://dx.doi.org/10.1182/blood.v96.2.647.

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Abstract In 21 patients with lymphoproliferative disease of granular lymphocytes (LDGL), we investigated the expression and the function of molecules belonging to TNF-receptor and TNF-ligand superfamilies (CD30/CD30L; CD40/CD40L; CD27/CD70; Fas [CD95]/FasL[CD95L]). Fourteen patients were characterized by a proliferation of granular lymphocytes (GLs) expressing the CD3+CD16+phenotype, whereas 7 cases showed the CD3−CD16+ CD56 ± phenotype. Our data show that both CD3+ and CD3-GLs are preferentially equipped with CD30, CD40, CD40L, CD70, and CD95 antigens; this pattern is usually associated with

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Conacher, Margaret, Robin Callard, Karen McAulay, et al. "Epstein-Barr Virus Can Establish Infection in the Absence of a Classical Memory B-Cell Population." Journal of Virology 79, no. 17 (2005): 11128–34. http://dx.doi.org/10.1128/jvi.79.17.11128-11134.2005.

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ABSTRACT Epstein-Barr virus (EBV) is a ubiquitous human herpesvirus that persists in the body for life after primary infection. The primary site of EBV persistence is the memory B lymphocyte, but whether the virus initially infects naïve or memory B cells is still disputed. We have analyzed EBV infection in nine cases of X-linked hyper-immunoglobulin M (hyper-IgM) syndrome who, due to a mutation in CD40 ligand gene, do not have a classical, class-switched memory B-cell population (IgD− CD27+). We found evidence of EBV infection in 67% of cases, which is similar to the infection rate found in

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Yoo, S. J., S. W. Kang, J. Kim, I. S. Yoo, C. K. Park, and H. R. Lee. "AB0109 THE ROLE OF CD70 IN THE DEVELOPMENT OF RHEUMATOID ARTHRITIS." Annals of the Rheumatic Diseases 79, Suppl 1 (2020): 1353.1–1355. http://dx.doi.org/10.1136/annrheumdis-2020-eular.2448.

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Background:Rheumatoid arthritis (RA) is a progressive, chronic inflammatory autoimmune disease. Pro-inflammatory molecules, activated lymphocytes, and the migration of inflammatory cells are important in the development of RA. There are many unknown causes of RA. And there are many patients who are refractory to treatment with known disease-modifying anti-rheumatic drugs. So, unknown cause of RA needs to be elucidated.CD70 is a member of the tumor necrosis factor (TNF) superfamily and a ligand for CD27. The interaction of CD70 with its receptor CD27 promotes expansion and differentiation of me

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Masamoto, Izumi, Sawako Horai, Tomohiro Kozako, et al. "CD70 Expression on HTLV-1 Infected T Cells of Carriers and ATL Patients and Its Clinical Significance." Blood 116, no. 21 (2010): 1730. http://dx.doi.org/10.1182/blood.v116.21.1730.1730.

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Abstract Abstract 1730 Human T-lymphotropic virus type-1(HTLV-1) is the causative agent of adult T cell leukemia/lymphoma (ATL). HTLV-1 infected T cell growth or leukemogenesis in ATL is controlled by various host immune surveillance systems. Among them, CD70 on HTLV-1 infected T cells coupled with CD27 on virus specific cytotoxic T cells has been suggested to play an important role in ATL leukemogenesis. The CD70 molecule is the only known ligand for CD27, a member of the tumor necrosis factor (TNF) receptor superfamily 7. This negative immunoregulatory pathway downregulates cytotoxic T lymph

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Powell, Daniel J., Mark E. Dudley, Paul F. Robbins, and Steven A. Rosenberg. "Transition of late-stage effector T cells to CD27+ CD28+ tumor-reactive effector memory T cells in humans after adoptive cell transfer therapy." Blood 105, no. 1 (2005): 241–50. http://dx.doi.org/10.1182/blood-2004-06-2482.

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Abstract In humans, the pathways of memory T-cell differentiation remain poorly defined. Recently, adoptive cell transfer (ACT) of tumor-reactive T lymphocytes to metastatic melanoma patients after nonmyeloablative chemotherapy has resulted in persistence of functional, tumor-reactive lymphocytes, regression of disease, and induction of melanocyte-directed autoimmunity in some responding patients. In the current study, longitudinal phenotypic analysis was performed on melanoma antigen-specific CD8+ T cells during their transition from in vitro cultured effector cells to long-term persistent me

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Dijke, E., K. Derkatz, J. Pearcey, F. Wong, B. Motyka, and L. West. "Cis-Binding of the Inhibitory Molecule CD22 to CD22 Ligand (CD22L) Controls Activation of Human CD27+IgM+ B Cells." Journal of Heart and Lung Transplantation 36, no. 4 (2017): S47. http://dx.doi.org/10.1016/j.healun.2017.01.111.

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Humphreys, Tricia L., Lee Ann Baldridge, Steven D. Billings, James J. Campbell, and Stanley M. Spinola. "Trafficking Pathways and Characterization of CD4 and CD8 Cells Recruited to the Skin of Humans Experimentally Infected with Haemophilus ducreyi." Infection and Immunity 73, no. 7 (2005): 3896–902. http://dx.doi.org/10.1128/iai.73.7.3896-3902.2005.

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ABSTRACT T-cell homing to infected skin is not well studied in humans. We examined sites experimentally infected with Haemophilus ducreyi by immunohistochemistry and flow cytometry for expression of receptors and ligands involved in cutaneous T-cell homing and determined the phenotypes of the T cells that trafficked to skin. Endothelial cells expressed E-selectin in infected but not uninfected skin, while peripheral node addressin (PNAd) was minimally expressed in all samples. CC chemokine ligand 27 (CCL27) was expressed in the epidermis and endothelium of both infected and uninfected skin. In

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Dijke, Esme, Kim Derkatz, Jean Pearcey, Fred Wong, Bruce Motyka, and Lori West. "Regulation of Human CD27+IgM+ B Cell Activation by Cis-Binding of the Inhibitory Molecule CD22 to CD22 Ligand (CD22L)." Transplantation 101 (May 2017): S5. http://dx.doi.org/10.1097/01.tp.0000520297.36145.fc.

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Kessel, Christoph, Wolfhart Kreuz, Katharina Brassat, Thomas Klingebiel, and Christoph Königs. "Ligand Mediated Targeting of FVIII Inhibitor Specific Primary B Cells Via Surface Immunoglobulin." Blood 106, no. 11 (2005): 3206. http://dx.doi.org/10.1182/blood.v106.11.3206.3206.

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Abstract Hemophilia A is an X-linked bleeding disorder. Mutations in the Factor VIII (FVIII) gene result in reduced or non-functional expression of FVIII. In hemophilia A recombinant (rFVIII) or plasma derived (pdFVIII) preparations are substituted to restore coagulation activity. However, a major problem of current treatment in hemophilia A is the development of an antibody response (inhibitors) to FVIIII. Various Immune Tolerance Therapies (ITTs) are being applied to overcome the FVIII specific immune response. In this study, phage displayed random peptide libraries were screened with variou

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Salzer, Ulrich, Chiara Bacchelli, Sylvie Buckridge, et al. "Relevance of biallelic versus monoallelic TNFRSF13B mutations in distinguishing disease-causing from risk-increasing TNFRSF13B variants in antibody deficiency syndromes." Blood 113, no. 9 (2009): 1967–76. http://dx.doi.org/10.1182/blood-2008-02-141937.

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Abstract TNFRSF13B encodes transmembrane activator and calcium modulator and cyclophilin ligand interactor (TACI), a B cell– specific tumor necrosis factor (TNF) receptor superfamily member. Both biallelic and monoallelic TNFRSF13B mutations were identified in patients with common variable immunodeficiency disorders. The genetic complexity and variable clinical presentation of TACI deficiency prompted us to evaluate the genetic, immunologic, and clinical condition in 50 individuals with TNFRSF13B alterations, following screening of 564 unrelated patients with hypogammaglobulinemia. We identifi

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De Re, Valli, Alessandro Pavan, Vito Racanelli, Silvia Sansonno, and Giuseppe Toffoli. "Clonal CD27+ CD19+ B-Cell Expansion through Inhibition of FCgIIR in HCV+ Lymphorpoliferative Disorders." Blood 112, no. 11 (2008): 4923. http://dx.doi.org/10.1182/blood.v112.11.4923.4923.

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Abstract HCV infection may or may not be associated with extra-hepatic manifestations such as type-II mixed cryoglobulinemia (MC), a clonal B cell proliferative disorder. In persistent HCV infection without MC a increase in serum immunoglobulins (Ig) is commonly observed. We found this increase is polyclonal and is determined primarily by increased levels of both HCV-specific and nonspecific IgG. Despite this hypergammaglobulinemia, memory CD27+ do not accumulate, depending on a heightened sensitivity of memory B cells to BCR-independent noncognate T cell help which speeds up their terminal di

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Brugnoni, Duilio, Paolo Airò, and Roberto Cattaneo. "CD70 (CD27 ligand) expression by synovial fluid CD4+ T lymphocytes in rheumatoid arthritis: Comment on the article by Kohen et al." Arthritis & Rheumatism 40, no. 6 (1997): 1186–87. http://dx.doi.org/10.1002/art.1780400635.

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