Soluble CD27 induces IgG production through activation of antigen‐primed B cells

Dang, Linh Vu Phuong; Nilsson, Anna; Ingelman-Sundberg, Hanna M.; Cagigi, Alberto; Gelinck, L. B. S.; Titanji, Kehmia; Milito, Angelo De; Grützmeier, Sven; Hedlund, Jonas; Kroon, F.P.; Chiodi, Francesca

doi:10.1111/j.1365-2796.2011.02444.x

Cited by 25 publications

(21 citation statements)

References 62 publications

(80 reference statements)

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“…One study using recombinant human sCD27 in vitro suggested that sCD27 could block CD27-mediated signaling and thereby have an inhibitory effect (29). In contrast, other studies showed that sCD27 shed by WM lymphoplasmacytic cells induced up-regulation of CD40L and APRIL on WM mast cells (14), and it also induced IgG production through the activation of antigen-primed B cells (30), suggesting that sCD27 may act agonistically in the process of immune activation. CD27 is expressed only on subsets of T, B, NK, and hematopoietic progenitor cells, and some subsets, such as late-stage T effector cells, lose CD27 expression (31).…”

Section: Discussionmentioning

confidence: 81%

Soluble CD27-Pool in Humans May Contribute to T Cell Activation and Tumor Immunity

Huang

Jochéms

Anderson

et al. 2013

The Journal of Immunology

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The interaction between CD27 and its ligand CD70 has been implicated in regulating cellular immune responses to cancer. Here we report on the role of soluble CD27 (sCD27) in T-cell activation and its elevation in the serum of cancer patients after immunotherapy. In vitro, sCD27 is preferentially derived from activated CD4+ T cells. Adding sCD27 to stimulated peripheral blood mononuclear cells increases T-cell activation and proliferation, and is associated with the immunological synapse-related proteins myosin IIA, HMGB1, and the TCR Vβ chain. The pool of serum sCD27 is shown to be greater in healthy donors than in cancer patients. However, metastatic cancer patients treated with immunotherapy showed a significant increase in the serum sCD27-pool post-therapy (p < 0.0005); there was also an increased trend towards an association between enhanced sCD27-pool post-therapy and overall survival (p = 0.022). The identification of sCD27 as an immune modulator associated with enhanced human T-cell activation in vitro and in vivo provides a rationale for developing new immunotherapeutic strategies aimed at enhancing sCD27 for treating cancer and potentially other diseases.

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Section: Discussionmentioning

confidence: 81%

Soluble CD27-Pool in Humans May Contribute to T Cell Activation and Tumor Immunity

Huang

Jochéms

Anderson

et al. 2013

The Journal of Immunology

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“…However, we cannot rule out that tissue processing, including the use of collagenase, might lead to some loss of CD27 on the B-cell surface. Further, CD27 cleavage has been reported during T- and B-cell activation [32]. However, CD27 − memory B-cells have been reported in other species.…”

Section: Discussionmentioning

confidence: 99%

Phenotypes and distribution of mucosal memory B-cell populations in the SIV/SHIV rhesus macaque model

Demberg¹,

Mohanram²,

Venzon³

et al. 2014

Clinical Immunology

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As vaccine-elicited antibodies have now been associated with HIV protective efficacy, a thorough understanding of mucosal and systemic B-cell development and maturation is needed. We phenotyped mucosal memory B-cells, investigated isotype expression and homing patterns, and defined plasmablasts and plasma cells at three mucosal sites (duodenum, jejunum and rectum) in rhesus macaques, the commonly used animal model for pre-clinical vaccine studies. Unlike humans, macaque mucosal memory B-cells lacked CD27 expression; only two sub-populations were present: naïve (CD21+CD27−) and tissue-like (CD21−CD27−) memory. Similar to humans, IgA was the dominant isotype expressed. The homing markers CXCR4, CCR6, CCR9 and α4β7 were differentially expressed between naïve and tissue-like memory B-cells. Mucosal plasmablasts were identified as CD19+CD20+/−HLA-DR+Ki-67+IRF4+CD138+/− and mucosal plasma cells as CD19+CD20−HLA-DR−Ki-67−IRF4+CD138+. Both populations were CD39+/−CD27−. Plasma cell phenotype was confirmed by spontaneous IgA secretion by ELISpot of positively-selected cells and J-chain expression by real-time PCR. Duodenal, jejunal and rectal samples were similar in B-cell memory phenotype, isotype expression, homing receptors and plasmablast/plasma cell distribution among the three tissues. Thus rectal biopsies adequately monitor B-cell dynamics in the gut mucosa, and provide a critical view of mucosal B-cell events associated with development of vaccine-elicited protective immune responses and SIV/SHIV pathogenesis and disease control.

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“…Many factors may contribute to the increased plasmablast/plasma cells in HIV-infected individuals. For example, in vitro , soluble CD27 binds to CD70 on B cells leading to activation of Blimp-1 and XBP-1, factors linking to B cells terminal differentiation and IgG production [64]. In the course of HIV infection, plasma levels of soluble CD27 are increased, correlated with disease progression [65] and serum levels of total IgG [64].…”

Section: Mechanisms For the Loss Of Classical Memory B Cellsmentioning

confidence: 99%

“…For example, in vitro , soluble CD27 binds to CD70 on B cells leading to activation of Blimp-1 and XBP-1, factors linking to B cells terminal differentiation and IgG production [64]. In the course of HIV infection, plasma levels of soluble CD27 are increased, correlated with disease progression [65] and serum levels of total IgG [64]. Moreover, T cells from HIV-infected individuals but not from healthy controls express CD70, the ligand for CD27, presumably could enhance the CD27/CD70 interaction, and lead to the memory B cells terminal differentiation [66].…”

Section: Mechanisms For the Loss Of Classical Memory B Cellsmentioning

confidence: 99%

HIV-associated memory B cell perturbations

Luo

Wan

et al. 2015

Vaccine

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Memory B-cell depletion, hyperimmunoglobulinemia, and impaired vaccine responses are the hallmark of B cell perturbations inhuman immunodeficiency virus (HIV) disease. Although B cells are not the targets for HIV infection, there is evidence for B cell, especially memory B cell dysfunction in HIV disease mediated by other cells or HIV itself. This review will focus on HIV-associated phenotypic and functional alterations in memory B cells. Additionally, we will discuss the mechanism underlying these perturbations and the effect of anti-retroviral therapy (ART) on these perturbations.

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Soluble CD27 induces IgG production through activation of antigen‐primed B cells

Cited by 25 publications

References 62 publications

Soluble CD27-Pool in Humans May Contribute to T Cell Activation and Tumor Immunity

Soluble CD27-Pool in Humans May Contribute to T Cell Activation and Tumor Immunity

Phenotypes and distribution of mucosal memory B-cell populations in the SIV/SHIV rhesus macaque model

HIV-associated memory B cell perturbations

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