The Expression of BAFF Is Controlled by IRF Transcription Factors

Sjöstrand, Maria; Johansson, Alina; Aqrawi, Lara A.; Olsson, Tomas; Wahren‐Herlenius, Marie; Espinosa, Alexander

doi:10.4049/jimmunol.1501061

Cited by 81 publications

(63 citation statements)

References 27 publications

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“…Nevertheless, it has become clear from these studies that BAFF production is triggered by stimulation with type I and II interferons, which corresponds with our results showing interferon-induced BAFF secretion from decidual stromal cells. Indeed, BAFF expression is directly downstream of type I IFN signaling and members of the IFN regulatory factor family regulate BAFF53. However, since neither cord blood nor maternal-derived decidual mononuclear cells produced BAFF when stimulated with either IFN-γ or IFN-α in the present study, circulating immune cells in the fetus and mother are most likely not the main source for cord blood BAFF levels.…”

Section: Discussionmentioning

confidence: 60%

IFN type I and II induce BAFF secretion from human decidual stromal cells

Lundell

Nordström

Andersson

et al. 2017

Sci Rep

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B cell activating factor (BAFF) is a critical cytokine for maturation of immature B cells. In murine lymph nodes, BAFF is mainly produced by podoplanin-expressing stromal cells. We have previously shown that circulating BAFF levels are maximal at birth, and that farmers’ children exhibit higher BAFF levels in cord blood than non-farmers’ children. Here, we sought to investigate whether maternal-derived decidual stromal cells from placenta secrete BAFF and examine what factors could stimulate this production. We found that podoplanin is expressed in decidua basalis and in the underlying villous tissue as well as on isolated maternal-derived decidual stromal cells. Decidual stromal cells produced BAFF when stimulated with IFN-γ and IFN-α, and NK cells and NK-T-like cells competent of IFN-γ production were isolated from the decidua. Finally, B cells at different maturational stages are present in decidua and all expressed BAFF-R, while stromal cells did not. These findings suggest that decidual stromal cells are a cellular source of BAFF for B cells present in decidua during pregnancy.

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Section: Discussionmentioning

confidence: 60%

IFN type I and II induce BAFF secretion from human decidual stromal cells

Lundell

Nordström

Andersson

et al. 2017

Sci Rep

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“…There are many genes known to be affected by downstream of IFN signalling, several of which were upregulated in our set of genes such as chemokines ( Ccl5, Ccl12, Cxcl9, Cxcl10 )2223, cytokines ( TNFSF13B )24, proteins involved in antigen presentation ( H2-Q8, H2-sg17, H2-Q7, H2-Q2, H2-Q5, H2-K1, H2-T23, H2-D1, H2-D4, H2Q5, H2T22, H2T23, H2T4 )25, transcription factors (STAT2, IRF1) and Interferon induced IFIT, IFITM and OAS (IFIT2, IFIT3, IFITM1, IFITM2, IFITM3, Oas1, Oas2, Oals1). Interestingly, Type I IFN receptor (IFNAR) exhibited upregulation in our dataset.…”

Section: Resultsmentioning

confidence: 99%

Transcriptomic profiling of microglia reveals signatures of cell activation and immune response, during experimental cerebral malaria

Capuccini

Lin

Talavera-López

et al. 2016

Sci Rep

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Cerebral malaria is a pathology involving inflammation in the brain. There are many immune cell types activated during this process, but there is little information on the response of microglia, in this severe complication. We examined microglia by genome wide transcriptomic analysis in a model of experimental cerebral malaria (ECM), in which C57BL/6 mice are infected with Plasmodium berghei ANKA. Thousands of transcripts were differentially expressed in microglia at two different time points during infection. Proliferation of microglia was a dominant feature before the onset of ECM, and supporting this, we observed an increase in numbers of these cells in the brain. When cerebral malaria symptoms were manifest, genes involved in immune responses and chemokine production were upregulated, which were possibly driven by Type I Interferon. Consistent with this hypothesis, in vitro culture of a microglial cell line with Interferon-β, but not infected red blood cells, resulted in production of several of the chemokines shown to be upregulated in the gene expression analysis. It appears that these responses are associated with ECM, as microglia from mice infected with a mutant P. berghei parasite (ΔDPAP3), which does not cause ECM, did not show the same level of activation or proliferation.

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“…At cytokine level, T1-IFNs can induce the production of B-cell activating factor (BAFF) by myeloid cells (238, 260, 261). BAFF induction confers a significant proportion of T1-IFN-mediated damage in SLE as supported by the observation that IFN-α administration induces disease in SLE-prone mice but fails to do so in B-cell-deficient and BAFF-deficient mice on the same background (262).…”

Section: T1-ifns the Th17 Response And Their Interactions In Autoimmmentioning

confidence: 99%

Interactions between Type 1 Interferons and the Th17 Response in Tuberculosis: Lessons Learned from Autoimmune Diseases

et al. 2017

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The classical paradigm of tuberculosis (TB) immunity, with a central protective role for Th1 responses and IFN-γ-stimulated cellular responses, has been challenged by unsatisfactory results of vaccine strategies aimed at enhancing Th1 immunity. Moreover, preclinical TB models have shown that increasing IFN-γ responses in the lungs is more damaging to the host than to the pathogen. Type 1 interferon signaling and altered Th17 responses have also been associated with active TB, but their functional roles in TB pathogenesis remain to be established. These two host responses have been studied in more detail in autoimmune diseases (AID) and show functional interactions that are of potential interest in TB immunity. In this review, we first identify the role of type 1 interferons and Th17 immunity in TB, followed by an overview of interactions between these responses observed in systemic AID. We discuss (i) the effects of GM-CSF-secreting Th17.1 cells and type 1 interferons on CCR2+ monocytes; (ii) convergence of IL-17 and type 1 interferon signaling on stimulating B-cell activating factor production and the central role of neutrophils in this process; and (iii) synergy between IL-17 and type 1 interferons in the generation and function of tertiary lymphoid structures and the associated follicular helper T-cell responses. Evaluation of these autoimmune-related pathways in TB pathogenesis provides a new perspective on recent developments in TB research.

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The Expression of BAFF Is Controlled by IRF Transcription Factors

Cited by 81 publications

References 27 publications

IFN type I and II induce BAFF secretion from human decidual stromal cells

IFN type I and II induce BAFF secretion from human decidual stromal cells

Transcriptomic profiling of microglia reveals signatures of cell activation and immune response, during experimental cerebral malaria

Interactions between Type 1 Interferons and the Th17 Response in Tuberculosis: Lessons Learned from Autoimmune Diseases

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