Cutting Edge: Importance of IL-6 and Cooperation between Innate and Adaptive Immune Receptors in Cellular Vaccination with B Lymphocytes

Bush, Tony J. Vanden; Buchta, Claire M.; Claudio, Jennifer; Bishop, Gail A.

doi:10.4049/jimmunol.0900968

Cited by 25 publications

(28 citation statements)

References 23 publications

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“…This is in contrast with the results of Vanden Bush et al [54] reporting successful protection from Lm infection 30 d after CD40-B cell vaccination. However, in their manuscript, they only look at protection and did not enumerate the number of CD8 + Tm cells generated.…”

Section: Discussioncontrasting

confidence: 99%

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CD40-Activated B Cells Can Efficiently Prime Antigen-Specific Naïve CD8+ T Cells to Generate Effector but Not Memory T cells

et al. 2012

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BackgroundThe identification of the signals that should be provided by antigen-presenting cells (APCs) to induce a CD8+ T cell response in vivo is essential to improve vaccination strategies using antigen-loaded APCs. Although dendritic cells have been extensively studied, the ability of other APC types, such as B cells, to induce a CD8+ T cell response have not been thoroughly evaluated.Methodology/Principal FindingsIn this manuscript, we have characterized the ability of CD40-activated B cells, stimulated or not with Toll-like receptor (TLR) agonists (CpG or lipopolysaccharide) to induce the response of mouse naïve CD8+ T cells in vivo. Our results show that CD40-activated B cells can directly present antigen to naïve CD8+ T cells to induce the generation of potent effectors able to secrete cytokines, kill target cells and control a Listeria monocytogenes infection. However, CD40-activated B cell immunization did not lead to the proper formation of CD8+ memory T cells and further maturation of CD40-activated B cells with TLR agonists did not promote the development of CD8+ memory T cells. Our results also suggest that inefficient generation of CD8+ memory T cells with CD40-activated B cell immunization is a consequence of reduced Bcl-6 expression by effectors and enhanced contraction of the CD8+ T cell response.ConclusionsUnderstanding why CD40-activated B cell immunization is defective for the generation of memory T cells and gaining new insights about signals that should be provided by APCs are key steps before translating the use of CD40-B cell for therapeutic vaccination.

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Section: Discussioncontrasting

confidence: 99%

“…The difference might also be explained by the protocol used to generate CD40-B cells. Indeed, Bishop's team used CD40-B cells that spent only one day in culture [54] while we used cells cultured for 4 days. We believe that our protocol is closer to what is currently developed for human B cell expansion [15], [20].…”

Section: Discussionmentioning

confidence: 99%

CD40-Activated B Cells Can Efficiently Prime Antigen-Specific Naïve CD8+ T Cells to Generate Effector but Not Memory T cells

et al. 2012

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“…Innate immune receptors are critical for myeloid cell function and regulation and are thus most intensively studied in this cell type. However, B cells also express most innate receptors, and are highly responsive to their signals (70), which can interact with signals from adaptive immune receptors such as the B-cell antigen receptor (BCR) (71–73) and CD40 (74–76). Thus, an important knowledge gap is whether TRAF3 plays similar or distinct roles in regulating innate immune receptors of B cells, compared to myeloid cells.…”

Section: Roles Of Traf3 In B Lymphocytesmentioning

confidence: 99%

Roles of tumor necrosis factor receptor associated factor 3 (TRAF3) and TRAF5 in immune cell functions

Hildebrand

Buchta

et al. 2011

Immunological Reviews

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102

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Summary A large and diverse group of receptors utilizes the family of cytoplasmic signaling proteins known as tumor necrosis factor receptor (TNFR)-associated factors (TRAFs). In recent years, there has been a resurgence of interest and exploration of the roles played by TRAF3 and TRAF5 in cellular regulation, particularly in cells of the immune system, the cell types of focus in this review. This work has revealed that TRAF3 and TRAF5 can play diverse roles for different receptors even in the same cell type, as well as distinct roles in different cell types. Evidence indicates that TRAF3 and TRAF5 play important roles beyond the TNFR-superfamily (SF) and viral mimics of its members, mediating certain innate immune receptor and cytokine receptor signals, and most recently, signals delivered by the T-cell receptor (TCR) signaling complex. Additionally, much research has demonstrated the importance of TRAF3-mediated cellular regulation via its cytoplasmic interactions with additional signaling proteins. In particular, we discuss below evidence for the participation by TRAF3 in a number of the regulatory post-translational modifications involving ubiquitin that are important in various signaling pathways.

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“…It was also found that B cells were required for optimal CD4 + and CD8 + T cell anti-tumor immunity, and depletion of therapeutic B cells enhanced tumor growth in mice 10 . In addition, B cells have recently been found to play an important role in resisting infectious pathogens 16, 17 .…”

Section: Introductionmentioning

confidence: 99%

Adoptive Transfer of Tumor Reactive B Cells Confers Host T-Cell Immunity and Tumor Regression

Lao

Pan

et al. 2011

Clinical Cancer Research

134

120

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Purpose We investigated the antitumor reactivity of adoptively transferred effector B cells and the mechanisms by which they may mediate tumor regression in a spontaneous metastases model. Experimental Design 4T1 breast cancer cells were inoculated into the flanks of syngeneic Balb/C mice to prime draining lymph nodes. Tumor-draining lymph nodes (TDLN) were harvested and B cells activated ex vivo with LPS and anti-CD40 mAb. These activated B cells were adoptively transferred into mice inoculated with 4T1 tumor in the mammary fat pad. The induction of host T cell immunity was evaluated. Results Activated 4T1 TDLN B cells secreted IgG in response to tumor cells which was immunologically specific. These activated B cells were capable of mediating specific lysis of tumor cells in vitro. Transfer of these activated B cells alone mediated the inhibition of spontaneous metastases to the lung. Examination of the host revealed that the transfer of these B cells resulted in the induction of tumor specific T cell immunity as measured by cytotoxicity and cytokine (IFNγ and GM-CSF) production. The combined transfer of activated T and B cells from TDLN resulted in tumor regression, which was greater than either cell population alone, with host B cells capable of producing IgG that mediated lysis of tumor in the presence of complement. Conclusions We have found that appropriately primed B cells can mediate tumor regression by itself and confers host T cell antitumor immunity. Furthermore, effector B cells can serve as a useful adjunct in adoptive T cell therapy.

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Cutting Edge: Importance of IL-6 and Cooperation between Innate and Adaptive Immune Receptors in Cellular Vaccination with B Lymphocytes

Abstract: Material

Cited by 25 publications

References 23 publications

CD40-Activated B Cells Can Efficiently Prime Antigen-Specific Naïve CD8+ T Cells to Generate Effector but Not Memory T cells

CD40-Activated B Cells Can Efficiently Prime Antigen-Specific Naïve CD8+ T Cells to Generate Effector but Not Memory T cells

Roles of tumor necrosis factor receptor associated factor 3 (TRAF3) and TRAF5 in immune cell functions

Adoptive Transfer of Tumor Reactive B Cells Confers Host T-Cell Immunity and Tumor Regression

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