BIP induces mice CD19 hi regulatory B cells producing IL-10 and highly expressing PD-L1, FasL

Tang, Youfa; Jiang, Qing; Ou, Yanghui; Zhang, Fan; Qing, Kai; Sun, Yuming; Lu, Wenjie; Zhu, Huifen; Gong, Feili; Lei, Ping; Shen, Guanxin

doi:10.1016/j.molimm.2015.10.017

Cited by 30 publications

(32 citation statements)

References 46 publications

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“…Recent studies have suggested that GRP78 shows potent immunomodulatory properties in an extracellular form (8–11). GRP78 has been defined as an RAMP to counterbalance the inflammatory effects of PAMPs and DAMPs (9).…”

Section: Discussionmentioning

confidence: 99%

“…Recombinant mouse GRP78 was prepared as described in our previous report (11). Briefly, a plasmid encoding the full length of mouse GRP78 was transformed into Escherichia coli BL21 to generate glutathione- S -transferase (GST)-GRP78.…”

Section: Methodsmentioning

confidence: 99%

“…Besides, the phenotype of these anti-inflammatory DCs was stable regardless of exposure to lipopolysaccharide (LPS) (10). We also reported that GRP78 can increase the frequency of regulatory B-cells that produce interleukin (IL)-10 and highly express programmed death-ligand 1 and Fas ligand, resulting in the suppression of T-cell proliferation (11). In addition, GRP78 can induce myeloid antigen-presenting cells to maintain a “tolerogenic signature” upon LPS stimulation (12).…”

Section: Introductionmentioning

confidence: 99%

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GRP78 Impairs Production of Lipopolysaccharide-Induced Cytokines by Interaction with CD14

et al. 2017

Front. Immunol.

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The 78-kDa glucose-regulated protein (GRP78) is a stress-inducible chaperone that resides primarily in the endoplasmic reticulum. GRP78 has been described to be released at times of cellular stress and as having extracellular properties that are anti-inflammatory or favor the resolution of inflammation. In the current study, we confirmed that GRP78 impaired the production of lipopolysaccharide-induced pro-inflammatory cytokines in GRP78-treated bone-marrow-derived dendritic cells (DCs). To explore the underlying mechanism, first of all, GRP78 was checked to be bound to the plasma membrane. Interestingly, such binding promoted endocytosis of toll-like receptor (TLR) 4 and reduction in TLR4 on the plasma surface had a key role in desensitization of GRP78-treated DCs to lipopolysaccharide. Given that cluster of differentiation (CD)14 is a crucial regulator of TLR4 endocytosis, interaction of GRP78 with CD14 was investigated next. Data showed that GRP78 co-localized with CD14 on the plasma membrane and glutathione-S-transferase-GRP78 precipitated CD14. In CD14 knockout mice, down-regulation of tumor necrosis factor-α and reduction in TLR4 on the plasma surface were abrogated in GRP78-treated DCs. Overall, these data suggested that GRP78 mediates endocytosis of TLR4 by targeting CD14 to favor the resolution of inflammation.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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GRP78 Impairs Production of Lipopolysaccharide-Induced Cytokines by Interaction with CD14

et al. 2017

Front. Immunol.

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“…Recombinant murine Grp78 was prepared as our previous report (17). Briefly, plasmid encoding full length of murine Grp78 was transformed into Escherichia coli BL21 to generate Grp78.…”

Section: Methodsmentioning

confidence: 99%

“…We previously reported that recombinant mouse Grp78 (rmGrp78) could program splenic B cells into CD19 hi FasL + /PD-L1 + IL-10-producing B cells to suppress T cell proliferation (17). Besides regulatory B cells, it is valuable to investigate whether Grp78 could program other murine antigen-presenting cells (APCs) into tolerogenic cells to prevent unwanted immune reactions in mice.…”

Section: Introductionmentioning

confidence: 99%

Glucose-Regulated Protein 78-Induced Myeloid Antigen-Presenting Cells Maintained Tolerogenic Signature upon LPS Stimulation

Yang

Zhang

et al. 2016

Front. Immunol.

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The 78-kDa glucose-regulated protein (Grp78) is stress-inducible chaperone that mostly reside in the endoplasmic reticulum. Grp78 has been described to be released at times of cellular stress and as having extracellular properties that are anti-inflammatory or favor the resolution of inflammation. As antigen-presenting cells (APCs) play a critical role in both the priming of adaptive immune responses and the induction of self-tolerance, herein, we investigated the effect of Grp78 on the maturation of murine myeloid APCs (CD11c+ cells). Results showed that CD11c+ cells could be bound by AF488-labeled Grp78 and that Grp78 treatment induced a tolerogenic phenotype comparable to immature cells. Furthermore, when exposed to lipopolysaccharide, Grp78-treated CD11c+ cells (DCGrp78) did not adopt a mature dendritic cell phenotype. DCGrp78-primed T cells exhibited reduced proliferation along with a concomitant expansion of CD4+CD25+FoxP3+ cells in pancreaticoduodenal lymph nodes and induction of T cell apoptosis in vitro and ex vivo. The above work suggests that Grp78 is an immunomodulatory molecule that could aid resolution of inflammation. It may thus contribute to induce durable tolerance to be of potential therapeutic benefit in transplanted allogeneic grafts and autoimmune diseases such as type I diabetes.

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Adoptive transfer of GRP78-treated dendritic cells alleviates insulitis in NOD mice

Zhou

Yang

et al. 2021

Journal of Leukocyte Biology

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The 78‐kDa glucose‐regulated protein (GRP78) has extracellular, anti‐inflammatory properties that can aid resolving inflammation. It has been established previously that GRP78 induced myeloid CD11c+ cell differentiation into distinct tolerogenic cells. This tolerance induction makes GRP78 a potential therapeutic agent for transplanted allogeneic grafts and autoimmune diseases, such as type 1 diabetes. In this research, it is revealed that rmGRP78‐treated NOD mice bone marrow‐derived CD11c+ cells (GRP78‐DCs) highly expressed B7‐H4 but down‐regulated CD86 and CD40, and retained a tolerogenic signature even after stimulation by LPS. In the assessment of in vivo therapeutic efficacy after the adoptive transfer of GRP78‐DCs into NOD mice, fluorescent imaging analyses revealed that the transfer specifically homed in inflamed pancreases, promoting β‐cell survival and alleviating insulitis in NOD mice. The adoptive transfer of GRP78‐DCs also helped reduce Th1, Th17, and CTL, suppressing inflammatory cytokine production in vivo. The findings suggest that adoptive GRP78‐DC transfer is critical to resolving inflammation in NOD mice and may have relevance in a clinical setting.

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BIP induces mice CD19 hi regulatory B cells producing IL-10 and highly expressing PD-L1, FasL

Cited by 30 publications

References 46 publications

GRP78 Impairs Production of Lipopolysaccharide-Induced Cytokines by Interaction with CD14

GRP78 Impairs Production of Lipopolysaccharide-Induced Cytokines by Interaction with CD14

Glucose-Regulated Protein 78-Induced Myeloid Antigen-Presenting Cells Maintained Tolerogenic Signature upon LPS Stimulation

Adoptive transfer of GRP78-treated dendritic cells alleviates insulitis in NOD mice

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