BAFF-secreting neutrophils drive plasma cell responses during emergency granulopoiesis

Parsa, Roham; Lund, Harald; Georgoudaki, Anna‐Maria; Zhang, Xingmei; Guerreiro-Cacais, André Ortlieb; Grommisch, David; Warnecke, Andreas; Croxford, Andrew L.; Jagodic, Maja; Becher, Burkhard; Karlsson, Mikael C. I.; Harris, Robert A.

doi:10.1084/jem.20150577

Cited by 70 publications

(76 citation statements)

References 50 publications

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“…In this regard, BAFF can act as a co-stimulatory molecule for T-cells and promote Th17 development (268, 269). BAFF can also directly activate plasma cells, which are not depleted by rituximab (270, 271). …”

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

confidence: 99%

“…Thirdly, T1-IFNs stimulate BAFF production, which is essential for T1-IFN-mediated pathogenic effects in mouse SLE (261, 262, 293). It is recently shown that IL-17 also induces BAFF production and that IL-17-driven, G-CSF-dependent PMN recruitment drives plasma cell responses during emergency granulopoiesis in a BAFF-dependent way (271). Also, therapeutically administered G-CSF, which is physiologically induced by IL-17, increases BAFF production by PMN (294).…”

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

confidence: 99%

“…Both T1-IFNs and IL-17 can induce BAFF expression, which contributes to disease in SLE as illustrated by the clinical successes of BAFF-inhibition (261, 271, 335). BAFF increases B-cell numbers and antibody titers (293, 336) and treatment with anti-BAFF in SLE patients reduces serum IgG levels (335).…”

Section: Interactions Between T1-ifns and Th17 Immunity In Tbmentioning

confidence: 99%

“…IL-17 stimulates the migration of PMN to lymphoid structures where they can produce large quantities of BAFF that directly drive plasma cell responses. Also, IL-17-induced G-CSF primes PMN for BAFF production upon activation (271, 294). Vice versa , elevated BAFF levels have been reported to increase Th17 immunity in AID and infection (268, 269, 343).…”

Section: Interactions Between T1-ifns and Th17 Immunity In Tbmentioning

confidence: 99%

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

confidence: 99%

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

confidence: 99%

Section: Interactions Between T1-ifns and Th17 Immunity In Tbmentioning

confidence: 99%

Section: Interactions Between T1-ifns and Th17 Immunity In Tbmentioning

confidence: 99%

See 2 more Smart Citations

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

et al. 2017

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“…Alternatively, the absence of IL-17R signaling could alter the activity of neutrophils recruited to the spleen after infection. A recent study has identified that IL-17 stimulated prostaglandin E2 production by stromal cells recruits BAFF-producing neutrophils to support B cell activation and survival (55). As we observed a decrease in expression of Cox2 , which promotes prostaglandin synthesis, by FRCs from Il-17ra −/− mice after infection, this could result in a decline in BAFF production by recruited neutrophils, leading to a subsequent decline in B cell numbers, specifically activated B cells undergoing plasmablast differentiation.…”

Section: Discussionmentioning

confidence: 99%

IL-17 Promotes Differentiation of Splenic LSK− Lymphoid Progenitors into B Cells following Plasmodium yoelii Infection

Ghosh

Brown

Stumhofer

2017

The Journal of Immunology

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LSK− (Lineage−Sca-1+c-kit−) cells are a lymphoid progenitor population that expands in the spleen and preferentially differentiates into mature B cells in response to Plasmodium yoelii infection in mice. Furthermore, LSK− derived B cells can subsequently contribute to the ongoing immune response through the generation of parasite-specific antibody secreting cells, and germinal center and memory B cells. However, the factors that promote their differentiation into B cells in the spleen after infection are not defined. Here we show that LSK− cells produce the cytokine IL-17 in response to Plasmodium infection. Using Il-17ra−/− mice IL-17R signaling in cells other than LSK− cells was found to support their differentiation into B cells. Moreover, primary splenic stromal cells grown in the presence of IL-17 enhanced the production of CXCL12, a chemokine associated with B-cell development in the bone marrow, by a population of IL-17RA–expressing podoplanin+CD31− stromal cells, a profile associated with fibroblastic reticular cells. Subsequent blockade of CXCL12 in vitro reduced differentiation of LSK− cells into B cells, supporting a direct role for this chemokine in this process. Immunofluorescence indicated that podoplanin+ stromal cells in the red pulp were the primary producers of CXCL12 after P. yoelii infection. Furthermore, podoplanin staining on stromal cells was more diffuse, and CXCL12 staining was dramatically reduced in Il-17ra−/− mice after infection. Together these results identify a distinct pathway that supports lymphoid development in the spleen during acute Plasmodium infection.

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The role of B cells in heart failure and implications for future immunomodulatory treatment strategies

et al. 2020

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Despite numerous demonstrations that the immune system is activated in heart failure, negatively affecting patients' outcomes, no definitive treatment strategy exists directed to modulate the immune system. In this review, we present the evidence that B cells contribute to the development of hypertrophy, inflammation, and maladaptive tissue remodelling. B cells produce antibodies that interfere with cardiomyocyte function, which culminates as the result of recruitment and activation of a variety of innate and structural cell populations, including neutrophils, macrophages, fibroblasts, and T cells. As B cells appear as active players in heart failure, we propose here novel immunomodulatory therapeutic strategies that target B cells and their products.

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BAFF-secreting neutrophils drive plasma cell responses during emergency granulopoiesis

Abstract: Harris and collaborators show that neutropenia results in increased formation of plasma cells and elevated antibody production.

Cited by 70 publications

References 50 publications

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

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

IL-17 Promotes Differentiation of Splenic LSK− Lymphoid Progenitors into B Cells following Plasmodium yoelii Infection

The role of B cells in heart failure and implications for future immunomodulatory treatment strategies

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