CD154-CD40 interactions in the control of murine B cell hematopoiesis

Carlring, Jennifer; Altaher, Hala M.; Clark, Susan J.; Chen, Xi; Latimer, Sarah L.; Jenner, Tracey J.; Buckle, Anne-Marie; Heath, Andrew W.

doi:10.1189/jlb.0310179

Cited by 11 publications

(9 citation statements)

References 42 publications

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“…Numerous studies have shown that EAMG is CD4 + T cell‐dependent and requires the co‐stimulatory molecules CD40L and CD40 on T and B cells, respectively . Both CD80 and CD86 are necessary for T cell activation and survival, while the interaction between CD40 and its ligand (CD40L) can activate resting B cells and enhance the expression of CD80 and CD86 . It has been reported that a B7‐deficiency can result in lower titres of the virus‐specific IgG2a response and a lack of an IgG1 response in mice infected with the vesicular stomatitis virus .…”

Section: Discussionmentioning

confidence: 99%

Delivery of an miR155 inhibitor by anti-CD20 single-chain antibody into B cells reduces the acetylcholine receptor-specific autoantibodies and ameliorates experimental autoimmune myasthenia gravis

Wang

Tian

Yan

et al. 2014

Clinical and Experimental Immunology

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SummaryMicroRNA-155 (miR155) is required for antibody production after vaccination with attenuated Salmonella. miR155-deficient B cells generated reduced germinal centre responses and failed to produce high-affinity immunoglobulin (Ig)G1 antibodies. In this study, we observed up-regulation of miR155 in the peripheral blood mononuclear cells (PBMCs) of patients with myasthenia gravis (MG), and miR155 was also up-regulated in torpedo acetylcholine receptor (T-AChR)-stimulated B cells. We used an inhibitor of miR155 conjugated to anti-CD20 single-chain antibody to treat both the cultured B cells and the experimental autoimmune MG (EAMG) mice. Our results demonstrated that silencing of miR155 by its inhibitor impaired the B cellactivating factor (BAFF)-R-related signalling pathway and reduced the translocation of nuclear factor (NF)-κB into the nucleus. Additionally, AChR-specific autoantibodies were reduced, which may be related to the altered amounts of marginal zone B cells and memory B cells in the spleens of EAMG mice. Our study suggests that miR155 may be a promising target for the clinical therapy of MG.

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Section: Discussionmentioning

confidence: 99%

Delivery of an miR155 inhibitor by anti-CD20 single-chain antibody into B cells reduces the acetylcholine receptor-specific autoantibodies and ameliorates experimental autoimmune myasthenia gravis

Wang

Tian

Yan

et al. 2014

Clinical and Experimental Immunology

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“…The signal transduction mediated by CD40-CD40L interaction could activate NF-κB, STAT3, MAPK, and other kinases ( Van Kooten and Banchereau, 2000 ; Elgueta et al., 2009 ). Accumulated studies have indicated that CD40 is responsible for promoting cellular and humoral adaptive immunity and inflammatory responses ( Van Kooten and Banchereau, 2000 ; Benveniste et al., 2004 ; Elgueta et al., 2009 ; Carlring et al., 2011 ). Besides, interaction of CD40 and CD40L between the DCs and CD4 + T cells triggers DCs to activate cytotoxic CD8 + cells ( Bennett et al., 1998 ; Ridge et al., 1998 ; Schoenberger et al., 1998 ).…”

Section: Regulators In Anti-malaria Immune Responsesmentioning

confidence: 99%

Accelerator or Brake: Immune Regulators in Malaria

Cai

Xiao

2020

Front. Cell. Infect. Microbiol.

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Malaria is a life-threatening infectious disease, affecting over 250 million individuals worldwide each year, eradicating malaria has been one of the greatest challenges to public health for a century. Growing resistance to anti-parasitic therapies and lack of effective vaccines are major contributing factors in controlling this disease. However, the incomplete understanding of parasite interactions with host anti-malaria immunity hinders vaccine development efforts to date. Recent studies have been unveiling the complexity of immune responses and regulators against Plasmodium infection. Here, we summarize our current understanding of host immune responses against Plasmodium-derived components infection and mainly focus on the various regulatory mechanisms mediated by recent identified immune regulators orchestrating anti-malaria immunity.

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“…CD40-mediated signal transduction activates multiple pathways, including those signaling through NFκB, STAT3 (Signal transducers and activators of transcription-3), MAPK (Mitogen-activated protein kinase), and other kinases [ 17 – 19 ]. CD40 is mostly known to function in the initiation and progression of cellular and humoral adaptive immunity, including T cell-dependent immunoglobulin class switching, memory B cell development, and germinal center formation [ 17 , 18 , 20 ]. Engagement of CD40 on macrophages and CD40L on T-cells has been shown to promote inflammatory responses in many neurologic diseases [ 21 ].…”

Section: Introductionmentioning

confidence: 99%

Increased CD40 Expression Enhances Early STING-Mediated Type I Interferon Response and Host Survival in a Rodent Malaria Model

Yao

Lin

et al. 2016

PLoS Pathog

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Both type I interferon (IFN-I) and CD40 play a significant role in various infectious diseases, including malaria and autoimmune disorders. CD40 is mostly known to function in adaptive immunity, but previous observations of elevated CD40 levels early after malaria infection of mice led us to investigate its roles in innate IFN-I responses and disease control. Using a Plasmodium yoelii nigeriensis N67 and C57BL/6 mouse model, we showed that infected CD40-/- mice had reduced STING and serum IFN-β levels day-2 post infection, higher day-4 parasitemia, and earlier deaths. CD40 could greatly enhance STING-stimulated luciferase signals driven by the IFN-β promoter in vitro, which was mediated by increased STING protein levels. The ability of CD40 to influence STING expression was confirmed in CD40-/- mice after malaria infection. Substitutions at CD40 TRAF binding domains significantly decreased the IFN-β signals and STING protein level, which was likely mediated by changes in STING ubiquitination and degradation. Increased levels of CD40, STING, and ISRE driven luciferase signal in RAW Lucia were observed after phagocytosis of N67-infected red blood cells (iRBCs), stimulation with parasite DNA/RNA, or with selected TLR ligands [LPS, poly(I:C), and Pam3CSK4]. The results suggest stimulation of CD40 expression by parasite materials through TLR signaling pathways, which was further confirmed in bone marrow derived dendritic cells/macrophages (BMDCs/BMDMs) and splenic DCs from CD40-/-, TLR3-/- TLR4-/-, TRIF-/-, and MyD88-/- mice after iRBC stimulation or parasite infection. Our data connect several signaling pathways consisting of phagocytosis of iRBCs, recognition of parasite DNA/RNA (possibly GPI) by TLRs, elevated levels of CD40 and STING proteins, increased IFN-I production, and longer host survival time. This study reveals previously unrecognized CD40 function in innate IFN-I responses and protective pathways in infections with malaria strains that induce a strong IFN-I response, which may provide important information for better understanding and management of malaria.

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CD154-CD40 interactions in the control of murine B cell hematopoiesis

Abstract: CD154 is expressed by radioresistant cells in the bone marrow, and plays a role in fine-tuning B cell hematopoiesis.

Cited by 11 publications

References 42 publications

Delivery of an miR155 inhibitor by anti-CD20 single-chain antibody into B cells reduces the acetylcholine receptor-specific autoantibodies and ameliorates experimental autoimmune myasthenia gravis

Delivery of an miR155 inhibitor by anti-CD20 single-chain antibody into B cells reduces the acetylcholine receptor-specific autoantibodies and ameliorates experimental autoimmune myasthenia gravis

Accelerator or Brake: Immune Regulators in Malaria

Increased CD40 Expression Enhances Early STING-Mediated Type I Interferon Response and Host Survival in a Rodent Malaria Model

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