All-trans-retinoic acid accelerates the differentiation of human B lymphocytes maturing into plasma cells

Morikawa, Keiko; Nonaka, Mitsuko

doi:10.1016/j.intimp.2005.06.002

Cited by 41 publications

(41 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Smith et al reported that Ag-specific IgG1 responses were drastically impaired in vitamin A-deficient mice (46). Morikawa et al demonstrated that the addition of exogenous retinoic acid to human B cell cultures enhanced the terminal differentiation of B cells into plasma cells (47). On the contrary, our study showed that treatment with ATRA reduced Ab production both in vitro and in vivo.…”

Section: Discussioncontrasting

confidence: 69%

See 1 more Smart Citation

Retinoic Acid Attenuates Rheumatoid Inflammation in Mice

Kwok

Park

Cho

et al. 2012

The Journal of Immunology

View full text Add to dashboard Cite

Retinoic acid is the active vitamin A derivative and is well-known to have diverse immunomodulatory actions. In this study, we investigated the impact of all-trans retinoic acid (ATRA), a biologic key metabolite of vitamin A, on the development of arthritis and the pathophysiologic mechanisms by which ATRA might have antiarthritic effects in animal model of rheumatoid arthritis (RA; collagen-induced arthritis [CIA] in DBA/1J mice). We showed that treatment with ATRA markedly suppressed the clinical and histologic signs of arthritis in the CIA mice. It reduced the expression of IL-17 in the arthritic joints. Interestingly, Foxp3+ regulatory T cells were markedly increased and IL-17–producing CD4+ T cells (Th17 cells) were decreased in the spleens of ATRA-treated mice. In vitro treatment with ATRA induced the expression of Foxp3 and repressed the IL-17 expression in the CD4+ T cells in mice. ATRA suppressed the production of total IgG and IgG2a in splenocytes that were stimulated by LPS. It also reduced serum levels of total IgG and IgG2 anti-collagen Abs and germinal center formation in CIA mice. In addition, the ATRA-treated mice showed decreased osteoclast formation in arthritic joints. Moreover, ATRA downregulated the expression of receptor activator of NF-κB ligand, the leading player of osteoclastogenesis, in the CD4+ T cells and fibroblast-like synoviocytes from patients with RA. Furthermore, ATRA prevented both human monocytes and mice bone marrow-derived monocytes/macrophage cells from differentiating into osteoclasts. These data suggest ATRA might be an effective treatment modality for RA patients.

show abstract

Section: Discussioncontrasting

confidence: 69%

“…When it comes to the impact of retinoic acid on humoral immune responses, a few reports have shown experimental evidence that retinoic acid might promote humoral immune responses (46,47). Smith et al reported that Ag-specific IgG1 responses were drastically impaired in vitamin A-deficient mice (46).…”

Section: Discussionmentioning

confidence: 99%

Retinoic Acid Attenuates Rheumatoid Inflammation in Mice

Kwok

Park

Cho

et al. 2012

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…Previous reports using several models have shown fairly consistently that CD40 ligation alone can induce B-cell proliferation in human and mouse B cells [4,33], and that CD40 ligation plus IL-4 can promote B-cell isotype switching to IgE and IgG1 [34]. RA has also been reported to increase Ig production by tonsillar B cells stimulated with anti-CD40 in the presence of IL-10 [15]. It is further believed that CD40 ligation along with IL-4 can augment the primary signal mediated by antigen binding to the BCR, allowing the processes of B-cell activation, survival and differentiation to proceed towards a productive humoral immune response [11,35].…”

Section: Introductionmentioning

confidence: 88%

“…All-trans-retinoic acid (RA), a natural bioactive metabolite of vitamin A [12], regulates a broad range of biologic processes through binding to specific nuclear retinoid receptors [13], present in many cells types including T and B cells [14,15]. RA is well known for its ability to inhibit cell proliferation and regulate the expression of a large number of genes [13].…”

Section: Introductionmentioning

confidence: 99%

Retinoic acid promotes mouse splenic B cell surface IgG expression and maturation stimulated by CD40 and IL-4

Chen

Ross

2007

Cellular Immunology

View full text Add to dashboard Cite

Retinoic acid (RA) increases antibody production in vivo but its role in B-cell activation is unclear. In a model of purified mouse splenic B cells stimulated by CD40 coreceptor (as a surrogate of T cell co-stimulation), IL-4, a principal Th-2 cytokine, and ligation of the B-cell antigen receptor, CD40 engagement or IL-4 alone induced B-cell activation indicated by increased Igγ1 germline transcripts, cell proliferation, and surface (s)IgG1 expression, while triple stimulation with the combination of anti-CD40/IL-4/anti-μ synergized to heighten B-cell activation. Although RA was growth inhibitory for anti-CD40-activated B cells, RA increased the proportion of B cells that had more differentiated phenotypes, such as expression of higher level of activation-induced deaminase, Blimp-1, CD138/ syndecan-1 and sIgG1. Overall, RA can promote B-cell maturation at the population level by increasing the number of sIgG1 and CD138 expressing cells, which may be related to the potentiation of humoral immunity in vivo.

show abstract

“…7A). These gene products include heparin-binding epidermal growth factor (EGF)-like growth factor (HBEGF), which binds CD138 (52) and was expressed by both APC and PMN, CXCL12, which recruits CXCR4-expressing PB and PC (53), and interleukin-10 (IL-10), IL-4, CD80, and ALDH1A2, which have all been reported to play a role in PC generation and maintenance (3,27,(54)(55)(56)(57)(58).…”

Section: Figmentioning

confidence: 99%

Influence of Plasma Cell Niche Factors on the Recruitment and Maintenance of IRF4 ^hi Plasma Cells and Plasmablasts in Vaccinated, Simian Immunodeficiency Virus-Infected Rhesus Macaques with Low and High Viremia

Shaw

Miller-Novak

Mohanram

et al. 2017

J Virol

View full text Add to dashboard Cite

In a recent study, we found that protection following simian immunodeficiency virus (SIV) exposure correlated with rectal plasma cell frequency in vaccinated female rhesus macaques. We sought to determine if the same macaques maintained high mucosal plasma cell frequencies postinfection and if this translated to reduced viremia. Although delayed SIV acquisition did not predict subsequent viral control, alterations existed in the distribution of plasma cells and plasmablasts between macaques that exhibited high or low viremia. Flow cytometric analysis of cells from rectal biopsy specimens, bone marrow, and mesenteric lymph nodes of vaccinated infected, unvaccinated infected, and uninfected macaques identified two main IRF4 hi subsets of interest: CD138 ϩ plasma cells, and CD138 Ϫ plasmablasts. In rectal tissue, plasma cell frequency positively correlated with plasma viremia and unvaccinated macaques had increased plasma cells and plasmablasts compared to vaccinated animals. Likewise, plasmablast frequency in the mesenteric lymph node correlated with viremia. However, in bone marrow, plasmablast frequency negatively correlated with viremia. Accordingly, low-viremic macaques had a higher frequency of both bone marrow IRF4 hi subsets than did animals with high viremia. Significant reciprocal relationships between rectal and bone marrow plasmablasts suggested that efficient trafficking to the bone marrow as opposed to the rectal mucosa was linked to viral control. mRNA expression analysis of proteins involved in establishment of plasma cell niches in sorted bone marrow and rectal cell populations further supported this model and revealed differential mRNA expression patterns in these tissues.IMPORTANCE As key antibody producers, plasma cells and plasmablasts are critical components of vaccine-induced immunity to human immunodeficiency virus type 1 (HIV-1) in humans and SIV in the macaque model; however, few have attempted to examine the role of these cells in viral suppression postinfection. Our results suggest that plasmablast trafficking to and retention in the bone marrow play a previously unappreciated role in viral control and contrast the potential contribution of mucosal plasma cells to mediate protection at sites of infection with that of bone marrow plasmablasts and plasma cells to control viremia during chronic infection. Manipulation of niche factors influencing the distribution and maintenance of these critical antibody-secreting cells may serve as potential therapeutic targets to enhance antiviral responses postvaccination and postinfection.

show abstract

All-trans-retinoic acid accelerates the differentiation of human B lymphocytes maturing into plasma cells

Cited by 41 publications

References 29 publications

Retinoic Acid Attenuates Rheumatoid Inflammation in Mice

Retinoic Acid Attenuates Rheumatoid Inflammation in Mice

Retinoic acid promotes mouse splenic B cell surface IgG expression and maturation stimulated by CD40 and IL-4

Influence of Plasma Cell Niche Factors on the Recruitment and Maintenance of IRF4 ^hi Plasma Cells and Plasmablasts in Vaccinated, Simian Immunodeficiency Virus-Infected Rhesus Macaques with Low and High Viremia

Contact Info

Product

Resources

About

All-trans-retinoic acid accelerates the differentiation of human B lymphocytes maturing into plasma cells

Cited by 41 publications

References 29 publications

Retinoic Acid Attenuates Rheumatoid Inflammation in Mice

Retinoic Acid Attenuates Rheumatoid Inflammation in Mice

Retinoic acid promotes mouse splenic B cell surface IgG expression and maturation stimulated by CD40 and IL-4

Influence of Plasma Cell Niche Factors on the Recruitment and Maintenance of IRF4 hi Plasma Cells and Plasmablasts in Vaccinated, Simian Immunodeficiency Virus-Infected Rhesus Macaques with Low and High Viremia

Contact Info

Product

Resources

About

Influence of Plasma Cell Niche Factors on the Recruitment and Maintenance of IRF4 ^hi Plasma Cells and Plasmablasts in Vaccinated, Simian Immunodeficiency Virus-Infected Rhesus Macaques with Low and High Viremia