CD25+ B-1a Cells Express Aicda

Kaku, Hiroaki; Holodick, Nichol E.; Tumang, Joseph R.; Rothstein, Thomas L.

doi:10.3389/fimmu.2017.00672

Cited by 5 publications

(3 citation statements)

References 29 publications

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“…Additionally, CD25 expression on IgD+ B-cells was found to decrease uPA levels, further alleviating sepsis mortality. As an immunoregulatory cell, CD25 + B cells can secrete anti-inflammatory factors such as IL-10 and TGF-β to participate in immune regulation ( 49 ). Interleukin-2 receptor-α (IL-2Rα, CD25) is upregulated on macrophages and lymphocytes by cytokines, such as interferon-γ, interleukin-2 and interleukin-3, or by nonspecific stimulation of human monocytes with lipopolysaccharides ( 50 , 51 ).…”

Section: Discussionmentioning

confidence: 99%

Dissecting the mediating role of cytokines in the interaction between immune traits and sepsis: insights from comprehensive mendelian randomization

Zheng,

Wang,

Wang

et al. 2024

Front. Immunol.

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BackgroundSepsis is a life-threatening organ dysfunction resulting from a dysregulated host response to infection, yet the potential causal relationship between the immunophenotype and sepsis remains unclear.MethodsGenetic variants associated with the immunophenotype served as instrumental variables (IVs) in Mendelian randomization (MR) to elucidate the causal impact of the immunophenotype on three sepsis outcomes. Additionally, a two-step MR analysis was conducted to identify significant potential mediators between the immunophenotype and three sepsis outcomes.ResultsOur MR analysis demonstrated a significant association between the immunophenotype and sepsis outcome, with 36, 36, and 45 the immunophenotype associated with the susceptibility, severity, and mortality of sepsis, respectively. Specifically, our analysis highlighted the CD14+ CD16+ monocyte phenotype as a significant factor across all three sepsis outcomes, with odds ratios (ORs) and corresponding confidence intervals (CIs) indicating its impact on sepsis (OR = 1.047, CI: 1.001-1.096), sepsis in Critical Care Units (OR = 1.139, CI: 1.014-1.279), and sepsis-related 28-day mortality (OR = 1.218, CI: 1.104-1.334). Mediation analyses identified seven cytokines as significant mediators among 91 potential cytokines, including interleukin-5 (IL-5), S100A12, TNF-related apoptosis-inducing ligand (TRAIL), T-cell surface glycoprotein CD6 isoform, cystatin D, interleukin-18 (IL-18), and urokinase-type plasminogen activator (uPA). Furthermore, reverse MR analysis revealed no causal effect of sepsis outcomes on the immunophenotype.ConclusionOur MR study suggests that the immunophenotype is significantly associated with the susceptibility, severity, and mortality of patient with sepsis, providing, for the first time, robust evidence of significant associations between immune traits and their potential risks. This information is invaluable for clinicians and patients in making informed decisions and merits further attention.

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Section: Discussionmentioning

confidence: 99%

Dissecting the mediating role of cytokines in the interaction between immune traits and sepsis: insights from comprehensive mendelian randomization

Zheng,

Wang,

Wang

et al. 2024

Front. Immunol.

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“…Notably, B2 cells do not produce GM-CSF [73,102]. The proposed main B1-cell subgroups are depicted in Figure 1B [60,65,68,78,[103][104][105][106][107][108]. However, it remains to be established whether these B1-cell subtypes in humans are committed subsets or adaptations of a multifunctional B1-precursor cell to the tissue environment.…”

Section: B1-cell Subsets Have Distinctive Phenotypes and Functionsmentioning

confidence: 99%

The Forgotten Brother: The Innate-like B1 Cell in Multiple Sclerosis

et al. 2022

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Multiple sclerosis (MS) is a neurodegenerative disease of the central nervous system (CNS), traditionally considered a chronic autoimmune attack against the insulating myelin sheaths around axons. However, the exact etiology has not been identified and is likely multi-factorial. Recently, evidence has been accumulating that implies that autoimmune processes underlying MS may, in fact, be triggered by pathological processes initiated within the CNS. This review focuses on a relatively unexplored immune cell—the “innate-like” B1 lymphocyte. The B1 cell is a primary-natural-antibody- and anti-inflammatory-cytokine-producing cell present in the healthy brain. It has been recently shown that its frequency and function may differ between MS patients and healthy controls, but its exact involvement in the MS pathogenic process remains obscure. In this review, we propose that this enigmatic cell may play a more prominent role in MS pathology than ever imagined. We aim to shed light on the human B1 cell in health and disease, and how dysregulation in its delicate homeostatic role could impact MS. Furthermore, novel therapeutic avenues to restore B1 cells’ beneficial functions will be proposed.

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“…In fact, AID expression is upregulated during extrafollicular TD and TI Ab responses and is thus not unique to the GC reaction ( 25 ). Interestingly, B-1a cells are known to upregulate AID expression upon LPS stimulation ( 31 32 ). The identities of T cell subsets in the TI Ab responses are discussed in detail in the subsequent sections.…”

Section: Ti Ab Responsementioning

confidence: 99%

Expansion and Sub-Classification of T Cell-Dependent Antibody Responses to Encompass the Role of Innate-Like T Cells in Antibody Responses

Park

Kim

2018

Immune Netw

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In addition to T cell-dependent (TD) Ab responses, T cells can also regulate T cell-independent (TI) B cell responses in the absence of a specific major histocompatibility complex (MHC) class II and antigenic peptide-based interaction between T and B cells. The elucidation of T cells capable of supporting TI Ab responses is important for understanding the cellular mechanism of different types of TI Ab responses. Natural killer T (NKT) cells represent 1 type of helper T cells involved in TI Ab responses and more candidate helper T cells responsible for TI Ab responses may also include γδ T cells and recently reported B-1 helper CD4+ T cells. Marginal zone (MZ) B and B-1 cells, 2 major innate-like B cell subsets considered to function independently of T cells, interact with innate-like T cells. Whereas MZ B and NKT cells interact mutually for a rapid response to blood-borne infection, peritoneal memory phenotype CD49dhighCD4+ T cells support natural Ab secretion by B-1 cells. Here the role of innate-like T cells in the so-called TI Ab response is discussed. To accommodate the involvement of T cells in the TI Ab responses, we suggest an expanded classification of TD Ab responses that incorporate cognate and non-cognate B cell help by innate-like T cells.

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CD25+ B-1a Cells Express Aicda

Cited by 5 publications

References 29 publications

Dissecting the mediating role of cytokines in the interaction between immune traits and sepsis: insights from comprehensive mendelian randomization

Dissecting the mediating role of cytokines in the interaction between immune traits and sepsis: insights from comprehensive mendelian randomization

The Forgotten Brother: The Innate-like B1 Cell in Multiple Sclerosis

Expansion and Sub-Classification of T Cell-Dependent Antibody Responses to Encompass the Role of Innate-Like T Cells in Antibody Responses

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