PD-1-expressing B cells suppress CD4+ and CD8+ T cells via PD-1/PD-L1-dependent pathway

Wang, Xufu; Wang, Guoqiang; Wang, Zenghua; Liu, Bin; Han, Na; Li, Jiao; Lu, Chunyang; Liu, Xinfeng; Zhang, Qin; Yang, Qingbo; Wang, Guo‐Ming

doi:10.1016/j.molimm.2019.02.009

Cited by 89 publications

(87 citation statements)

References 20 publications

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“…Moreover, the modulating effect of IL-10 on B cells was already demonstrated in earlier studies 72,73 , whether IL-10 influences directly the expression of cell inhibitory molecules e.g. PD-L1, FasL, to increase cell contact-dependent suppressive activity of B cells 41,43,[74][75][76] , is currently unknown but suggested by previous publications showing an IL-10-inducible PD-L1 expression on monocytes 77,78 . Another possibility is that IL-10 is able to directly affect T cell suppression, but only in the presence of signaling from cell inhibitory molecules; however, this needs further investigation.…”

Section: Discussionmentioning

confidence: 83%

“…7d). In addition to IL-10, Bregs impair T cell function via surface proteins such as PD-L1 40,41 and FasL 42,43 . Therefore, we determined, whether Bregs generated by TLR9 activation show enhanced expression of these proteins.…”

Section: Regulatory B Cells Can Inhibit or Suppress Inflammation Medimentioning

confidence: 99%

“…Besides IL-10 secretion, the immunosuppressive capacity or checkpoint activity of regulatory B cells has also been associated with the production of IL-35 38 , TGF-ß 39 and inhibitory costimulatory molecules e.g. PD-L1 40,41 and FasL 42,43 .…”

Section: Introductionmentioning

confidence: 99%

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TLR9-activated B cells improve their regulatory function by endogenously produced catecholamines

Honke

Lowin

Opgenoorth

et al. 2020

Preprint

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The sympathetic nervous system (SNS) contributes to immune balance by promoting antiinflammatory B cells. However, whether B cells possess a self-regulating mechanism by which they modulate regulatory B cell (Breg) function is not well understood. In this study, we investigated the ability of B cells to synthesize catecholamines upon stimulation with different B cell activators. We found, that expression of the enzymes required to generate catecholamines, is upregulated by TLR9. TLR-9-specific expression of tyrosine hydroxylase (TH) correlated with upregulation of adrenergic receptors, enhanced IL-10 production, and with an overexpression of the co-inhibitory ligands PD-L1 and FasL. Moreover, concomitant stimulation of ß1-3-adrenergic receptors together with a BCR/TLR9 stimulus enhances the anti-inflammatory potential of Bregs to suppress CD4 T cells, a crucial population in the pathogenesis of autoimmune diseases, like rheumatoid arthritis. In conclusion, our data show that B cells possess autonomous mechanisms to modulate their regulatory function. These findings help to better understand the function of Bregs in autoimmune diseases and the interplay of sympathetic nervous system and B cell function.3 Introduction:

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Section: Discussionmentioning

confidence: 83%

Section: Regulatory B Cells Can Inhibit or Suppress Inflammation Medimentioning

confidence: 99%

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TLR9-activated B cells improve their regulatory function by endogenously produced catecholamines

Honke

Lowin

Opgenoorth

et al. 2020

Preprint

View full text Add to dashboard Cite

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“…Whether ectopic germinal centers are 290 present in the brain with cryptococcal meningitis, which has a prominent component in 291 the brain parenchyma, as were identified with neurosyphilis (40) was increased on activated B cells, particularly CD27+ and tissue-like memory cells, as 307 reported by others (43,45). Indeed, microbial antigens, modeled by toll-like receptor-9 to its effects on T cells, PD-1 on B cells can inhibit B cell activation, suppress B cell 310 proliferation and impair B cell inflammatory cytokine responses (12,13,45,47). 311…”

Section: Pd-1 Plasmablasts/plasma Cells Expression Subjects With Thementioning

confidence: 81%

“…including plasma cells, modulate the activity of other immune cells in the local 120 environment (4), as may B cells expressing surface immunomodulatory molecules such 121 as PD-1 (12,13). 122…”

Section: Introduction 101mentioning

confidence: 99%

B cell Compartmentalization in Blood and Cerebrospinal Fluid of HIV-Infected Ugandans with Cryptococcal Meningitis

Okurut

Meya

Bwanga

et al. 2019

Preprint

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“Find Me” and “Eat Me” signals: tools to drive phagocytic processes for modulating antitumor immunity

Xiao,

Zhang,

Guo

et al. 2024

Cancer Communications

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Phagocytosis, a vital defense mechanism, involves the recognition and elimination of foreign substances by cells. Phagocytes, such as neutrophils and macrophages, rapidly respond to invaders; macrophages are especially important in later stages of the immune response. They detect “find me” signals to locate apoptotic cells and migrate toward them. Apoptotic cells then send “eat me” signals that are recognized by phagocytes via specific receptors. “Find me” and “eat me” signals can be strategically harnessed to modulate antitumor immunity in support of cancer therapy. These signals, such as calreticulin and phosphatidylserine, mediate potent pro‐phagocytic effects, thereby promoting the engulfment of dying cells or their remnants by macrophages, neutrophils, and dendritic cells and inducing tumor cell death. This review summarizes the phagocytic “find me” and “eat me” signals, including their concepts, signaling mechanisms, involved ligands, and functions. Furthermore, we delineate the relationships between “find me” and “eat me” signaling molecules and tumors, especially the roles of these molecules in tumor initiation, progression, diagnosis, and patient prognosis. The interplay of these signals with tumor biology is elucidated, and specific approaches to modulate “find me” and “eat me” signals and enhance antitumor immunity are explored. Additionally, novel therapeutic strategies that combine “find me” and “eat me” signals to better bridge innate and adaptive immunity in the treatment of cancer patients are discussed.

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PD-1-expressing B cells suppress CD4+ and CD8+ T cells via PD-1/PD-L1-dependent pathway

Cited by 89 publications

References 20 publications

TLR9-activated B cells improve their regulatory function by endogenously produced catecholamines

TLR9-activated B cells improve their regulatory function by endogenously produced catecholamines

B cell Compartmentalization in Blood and Cerebrospinal Fluid of HIV-Infected Ugandans with Cryptococcal Meningitis

“Find Me” and “Eat Me” signals: tools to drive phagocytic processes for modulating antitumor immunity

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