Aberrant expression of BAFF in T cells of systemic lupus erythematosus, which is recapitulated by a human T cell line, Loucy

Yoshimoto, Keiko; Takahashi, Yasue; Ogasawara, M; Setoyama, Yumiko; Suzuki, Katsuya; Tsuzaka, Kensei; Abe, Tohru; Takeuchi, Tsutomu

doi:10.1093/intimm/dxl053

Cited by 43 publications

(40 citation statements)

References 43 publications

(32 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Indeed, in patients with SLE even T cells express abundant BAFF, in particular when they are activated (25). Attempts to correlate disease activity with the titer of circulating BAFF have largely failed, although a correlation between disease activity and the levels of BAFF and APRIL messenger RNA (mRNA) in whole blood cells has been shown (1,2,5).…”

Section: Discussionmentioning

confidence: 99%

Systemic activation of the immune system induces aberrant BAFF and APRIL expression in B cells in patients with systemic lupus erythematosus

Chu¹,

Enghard²,

Schürer³

et al. 2009

Arthritis & Rheumatism

104

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Systemic activation of the immune system induces aberrant BAFF and APRIL expression in B cells in patients with systemic lupus erythematosus

Chu¹,

Enghard²,

Schürer³

et al. 2009

Arthritis & Rheumatism

104

View full text Add to dashboard Cite

show abstract

“…Yoshimoto et al [47] reported that the inhibitors of p38 and JNK inhibited sBAFF production in 12-Otetradecanoylphorbol 13-acetate-and ionomycin-stimulated Loucy, a human T cell line. However, they showed only sBAFF secretion by ELISA [47]. Therefore, to verify the difference in data between the two analytical methods, we additionally analyzed it by flow cytometry.…”

Section: Discussionmentioning

confidence: 99%

“…6B). It has been known that sBAFF release is mediated by furin [4,32,46,47]. Therefore, to evaluate whether the JNK and p38 signaling pathways are involved in furin expression, we performed Western blot analysis.…”

Section: The Release Of Sbaff In Gmix-treated Bv-2 Cells Is Dependentmentioning

confidence: 99%

Functional implication of BAFF synthesis and release in gangliosides-stimulated microglia

Kim

Park

Jou

et al. 2009

Journal of Leukocyte Biology

View full text Add to dashboard Cite

BAFF is a recently identified member of the TNF ligand superfamily that plays a critical role in B cell differentiation, survival, and regulation of Ig production. In the present study, we examined whether BAFF is expressed in microglia, and the expression and release of BAFF are regulated by gangliosides. The results showed that BAFF was expressed and released in rat primary microglia as well as in BV-2 cells. Furthermore, its expression and release were increased by gangliosides stimulation and regulated by JAK-STAT, especially the STAT1-and STAT3-dependent signaling pathways. It was of particular interest to observe that SP600125 and SB203580, specific inhibitors of JNK and p38, did not inhibit BAFF synthesis but inhibited the release of sBAFF in gangliosides-treated cells by regulating furin expression, suggesting that the JNK and p38 signaling pathways regulate the release but not the synthesis of BAFF. Moreover, BV-2 cells expressed BAFF-R on their cell surface, and rat primary microglia expressed BAFF-R and TACI on their cell surface. rBAFF increased the release of cytokines, especially IL-6, TNF-␣, and IL-10, in rat primary microglia as well as in BV-2 cells. These findings imply that BAFF secreted by microglia may play important roles in CNS inflammation by regulating microglia as well as infiltrated B cells.

show abstract

“…BAFF/BLyS production by T cells was previously shown in patients with systemic lupus erythematosis. 38 In non-autoimmune mouse strains, BAFF/BLyS is produced mostly by dendritic cells and macrophages. 39 The presence of a large percentage of T cells producing BAFF/BLyS when NZB/W mice were injected with IgG2a may constitute a deregulation of BAFF/BLyS production as the result of an inherent over/ underexpression of a special class of molecules belonging to the Fc c-receptor family in those mice.…”

Section: Discussionmentioning

confidence: 99%

Long‐term administration of IgG2a anti‐NK1.1 monoclonal antibody ameliorates lupus‐like disease in NZB/W mice in spite of an early worsening induced by an IgG2a‐dependent BAFF/BLyS production

et al. 2008

View full text Add to dashboard Cite

Summary The role of natural killer (NK) T cells in the development of lupus‐like disease in mice is still controversial. We treated NZB/W mice with anti‐NK1.1 monoclonal antibodies (mAbs) and our results revealed that administration of either an irrelevant immunoglobulin G2a (IgG2a) mAb or an IgG2a anti‐NK1.1 mAb increased the production of anti‐dsDNA antibodies in young NZB/W mice. However, the continuous administration of an anti‐NK1.1 mAb protected aged NZB/W mice from glomerular injury, leading to prolonged survival and stabilization of the proteinuria. Conversely, the administration of the control IgG2a mAb led to an aggravation of the lupus‐like disease. Augmented titres of anti‐dsDNA in NZB/W mice, upon IgG2a administration, correlated with the production of BAFF/BLyS by dendritic, B and T cells. Treatment with an anti‐NK1.1 mAb reduced the levels of interleukin‐16, produced by T cells, in spleen cell culture supernatants from aged NZB/W. Adoptive transfer of NK T cells from aged to young NZB/W accelerated the production of anti‐dsDNA in recipient NZB/W mice, suggesting that NK T cells from aged NZB/W are endowed with a B‐cell helper activity. In vitro studies, using purified NK T cells from aged NZB/W, showed that these cells provided helper B‐cell activity for the production of anti‐dsDNA. We concluded that NK T cells are involved in the progression of lupus‐like disease in mature NZB/W mice and that immunoglobulin of the IgG2a isotype has an enhancing effect on antibody synthesis due to the induction of BAFF/BLyS, and therefore have a deleterious effect in the NZB/W mouse physiology.

show abstract

Aberrant expression of BAFF in T cells of systemic lupus erythematosus, which is recapitulated by a human T cell line, Loucy

Cited by 43 publications

References 43 publications

Systemic activation of the immune system induces aberrant BAFF and APRIL expression in B cells in patients with systemic lupus erythematosus

Systemic activation of the immune system induces aberrant BAFF and APRIL expression in B cells in patients with systemic lupus erythematosus

Functional implication of BAFF synthesis and release in gangliosides-stimulated microglia

Long‐term administration of IgG2a anti‐NK1.1 monoclonal antibody ameliorates lupus‐like disease in NZB/W mice in spite of an early worsening induced by an IgG2a‐dependent BAFF/BLyS production

Contact Info

Product

Resources

About