An Overview of B-1 Cells as Antigen-Presenting Cells

Popi, Ana Flávia; Longo-Maugéri, Ieda Maria; Mariano, Mário

doi:10.3389/fimmu.2016.00138

Cited by 70 publications

(60 citation statements)

References 79 publications

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“…B-1 cells from the peritoneal cavity migrate to inflammatory and/or infectious sites and release a series of immunomodulatory factors into the environment and also have the ability to differentiate into phagocytes[2,32]. Our group recently demonstrated a role for B-1 cell-derived phagocytes (B-1CDP) in L. major infection in vitro [13].…”

Section: Discussionmentioning

confidence: 99%

B-1 cells modulate the murine macrophage response toLeishmania majorinfection

Arcanjo

Nunes

Silva-Junior

et al. 2017

WJBC

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AIMTo investigate the modulatory effect of B-1 cells on murine peritoneal macrophages infected with Leishmania major (L. major) in vitro.METHODSPeritoneal macrophages obtained from BALB/c and BALB/c XID mice were infected with L. major and cultured in the presence or absence of B-1 cells obtained from wild-type BALB/c mice. Intracellular amastigotes were counted, and interleukin-10 (IL-10) production was quantified in the cellular supernatants using an enzyme-linked immunosorbent assay. The levels of the lipid mediator prostaglandin E2 (PGE2) were determined using a PGE2 enzyme immunoassay kit (Cayman Chemical, Ann Arbor, MI), and the number of lipid bodies was quantified in the cytoplasm of infected macrophages in the presence and absence of B-1 cells. Culturing the cells with selective PGE2-neutralizing drugs inhibited PGE2 production and confirmed the role of this lipid mediator in IL-10 production. In contrast, we demonstrated that B-1 cells derived from IL-10 KO mice did not favor the intracellular growth of L. major.RESULTSWe report that B-1 cells promote the growth of L. major amastigotes inside peritoneal murine macrophages. We demonstrated that the modulatory effect was independent of physical contact between the cells, suggesting that soluble factor(s) were released into the cultures. We demonstrated in our co-culture system that B-1 cells trigger IL-10 production by L. major-infected macrophages. Furthermore, the increased secretion of IL-10 was attributed to the presence of the lipid mediator PGE2 in supernatants of L. major-infected macrophages. The presence of B-1 cells also favors the production of lipid bodies by infected macrophages. In contrast, we failed to obtain the same effect on parasite replication inside L. major-infected macrophages when the B-1 cells were isolated from IL-10 knockout mice.CONCLUSIONOur results show that elevated levels of PGE2 and IL-10 produced by B-1 cells increase L. major growth, as indicated by the number of parasites in cell cultures.

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Section: Discussionmentioning

confidence: 99%

B-1 cells modulate the murine macrophage response toLeishmania majorinfection

Arcanjo

Nunes

Silva-Junior

et al. 2017

WJBC

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“…The stromal cells of the FALCs express high levels of the CXCL13 chemokine which facilitates the retention of B‐1 cells within the peritoneal cavity and supports their proliferation and germinal centre formation . B‐1 cells respond to T‐independent antigens and are further classified into CD5 + B‐1a cells and CD5 − B‐1b cells . B‐1 cells produce natural antibodies, mostly IgM, with anti‐inflammatory functions .…”

Section: Adaptive Immune Responsesmentioning

confidence: 99%

“…19 B-1 cells respond to T-independent antigens and are further classified into CD5 + B-1a cells and CD5 − B-1b cells. 176,177 B-1 cells produce natural antibodies, mostly IgM, with anti-inflammatory functions. 178,179 HFD in Id3 Bcell KO mice, which have increased numbers of B-1b cells and impaired Ag-specific antibody response, causes a decreased AT inflammation in an IgM-dependent manner.…”

Section: B Cellsmentioning

confidence: 99%

An update on immune dysregulation in obesity‐related insulin resistance

2019

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Obesity is associated with chronic low‐grade inflammation of the adipose tissue (AT) that might develop into systemic inflammation, insulin resistance (IR) and an increased risk of type 2 diabetes mellitus (T2DM) in severe obese rodents and humans. In the lean state, small normal adipocytes and AT macrophages interact with each other to maintain metabolic homeostasis but during obesity, enlarged adipocytes secrete inflammatory mediators and express immune receptors to recruit immune cells and aggravate the inflammation. The better understanding of the obesity‐related inflammatory milieu and the sequential events leading to IR could be helpful in designing new preventive and therapeutic strategies. The present review will discuss the cellular and molecular abnormalities participating in the pathogenesis of obesity in obese individuals as well as high‐fat diet (HFD)‐fed mice, a mouse model of obesity.

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“…The role of conventional B cells as antigen-presenting cells (APC) has been established in the 1980s’ (see [14] for an excellent discussion), and their contribution to the immune response is non-redundant with that of professional APCs. First, B cells present only specific Ag that they internalize through their B cell receptor (BCR), ensuring a linked recognition with cognate CD4 + T cells that is crucial for a coordinated immune response.…”

Section: B Cell Vs DC Activation Of Cd4+ T Cells In Lupusmentioning

confidence: 99%

B cell contribution of the CD4⁺T cell inflammatory phenotypes in systemic lupus erythematosus

Choi

Morel

2017

Autoimmunity

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Systemic lupus erythematosus is an autoimmune disease in which the effector molecules responsible for tissue damage are antibodies directed against a large number of self-antigens, among which nucleic acids complexed with proteins play a prominent role. These pathogenic autoantibodies are produced by plasma cells differentiated from activated autoreactive B cells, a process that requires complex interactions between multiple components of the immune systems. A key step in the activation of autoreactive B cells is provided by CD4+ T cells through cytokines and cell-to-cell contact. Lupus CD4+ T cells are autoreactive and they present an activated inflammatory phenotype that has been shown to contribute to disease. In addition to their role in antibody production, B cells have other effector functions, the most important ones being antigen presentation to and co-stimulation of CD4+ T cells, as well as the secretion of cytokines. Here we review what is known, largely based on mouse models, how these B cell effector functions contribute to the CD4+ T cell inflammatory phenotypes in lupus. When possible, we compare CD4+ T cell activation by B cells and by dendritic cells, and speculate how these interactions may contribute to the disease process.

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An Overview of B-1 Cells as Antigen-Presenting Cells

Cited by 70 publications

References 79 publications

B-1 cells modulate the murine macrophage response toLeishmania majorinfection

B-1 cells modulate the murine macrophage response toLeishmania majorinfection

An update on immune dysregulation in obesity‐related insulin resistance

B cell contribution of the CD4⁺T cell inflammatory phenotypes in systemic lupus erythematosus

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An Overview of B-1 Cells as Antigen-Presenting Cells

Cited by 70 publications

References 79 publications

B-1 cells modulate the murine macrophage response toLeishmania majorinfection

B-1 cells modulate the murine macrophage response toLeishmania majorinfection

An update on immune dysregulation in obesity‐related insulin resistance

B cell contribution of the CD4+T cell inflammatory phenotypes in systemic lupus erythematosus

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Product

Resources

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B cell contribution of the CD4⁺T cell inflammatory phenotypes in systemic lupus erythematosus