B lymphocytes trigger monocyte mobilization and impair heart function after acute myocardial infarction

Zouggari, Yasmine; Ait‐Oufella, Hafid; Bonnin, Philippe; Simon, Tabassome; Sage, Andrew P.; Guérin, Coralie L.; Vilar, José; Caligiuri, Giuseppina; Tsiantoulas, Dimitrios; Laurans, Ludivine; Dumeau, Edouard; Kotti, Salma; Bruneval, Patrick; Charo, Israel F.; Binder, Christoph J.; Danchin, Nicolás; Tedgui, Alain; Tedder, Thomas F.; Silvestre, Jean‐Sébastien; Mallat, Ziad

doi:10.1038/nm.3284

Cited by 460 publications

(469 citation statements)

References 44 publications

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“…Administration of clodronate-liposomes depletes phagocytes, predominately MØ (20, 53) (confirmed by F4/80 staining), indicating B cell-MØ communication in the amelioration of colitis. There are few data on B cell-MØ cross-talk, but it is not unprecedented; peritoneal MØ from B cell-deficient mice produced more TNF-a and IL-1b in response to LPS (54), and monocyte recruitment in murine myocardial infarction was triggered by B cells (55). The current study demonstrates B cell-MØ cooperation in the suppression of colitis.…”

Section: Discussionmentioning

confidence: 60%

Splenic B Cells fromHymenolepis diminuta–Infected Mice Ameliorate Colitis Independent of T Cells and via Cooperation with Macrophages

Reyes

Wang

Fernando

et al. 2015

The Journal of Immunology

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Helminth parasites provoke multicellular immune responses in their hosts that can suppress concomitant disease. The gut lumen-dwelling tapeworm Hymenolepis diminuta, unlike other parasites assessed as helminth therapy, causes no host tissue damage while potently suppressing murine colitis. With the goal of harnessing the immunomodulatory capacity of infection with H. diminuta, we assessed the putative generation of anti-colitic regulatory B cells following H. diminuta infection. Splenic CD19+ B cells isolated from mice infected 7 [HdBc(7d)] and 14 d (but not 3 d) previously with H. diminuta and transferred to naive mice significantly reduced the severity of dinitrobenzene sulfonic acid (DNBS)-, oxazolone-, and dextran-sodium sulfate–induced colitis. Mechanistic studies with the DNBS model, revealed the anti-colitic HdBc(7d) was within the follicular B cell population and its phenotype was not dependent on IL-4 or IL-10. The HdBc(7d) were not characterized by increased expression of CD1d, CD5, CD23, or IL-10 production, but did spontaneously, and upon LPS plus anti-CD40 stimulation, produce more TGF-β than CD19+ B cells from controls. DNBS-induced colitis in RAG1−/− mice was inhibited by administration of HdBc(7d), indicating a lack of a requirement for T and B cells in the recipient; however, depletion of macrophages in recipient mice abrogated the anti-colitic effect of HdBc(7d). Thus, in response to H. diminuta, a putatively unique splenic CD19+ B cell with a functional immunoregulatory program is generated that promotes the suppression of colitis dominated by TH1, TH2, or TH1-plus-TH2 events, and may do so via the synthesis of TGF-β and the generation of, or cooperation with, a regulatory macrophage.

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Section: Discussionmentioning

confidence: 60%

Splenic B Cells fromHymenolepis diminuta–Infected Mice Ameliorate Colitis Independent of T Cells and via Cooperation with Macrophages

Reyes

Wang

Fernando

et al. 2015

The Journal of Immunology

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“…The role of B-cells after MI was recently investigated using several B-cell ablation strategies in a permanent MI mouse model. 19 Applying an antibody against the CD20 antigen ablated both follicular and marginal B-cells but not B1 cells. This treatment reduced infarct size, lessened left ventricular dilation, and improved recovery of left ventricular function, as determined 14 days after MI.…”

Section: Role Of B-cells After MImentioning

confidence: 99%

“…18 Flow cytometry shows that myocardial B220 + B-cells were CD19 + IgD + IgM low , indicating that MI triggers the infiltration of circulating mature B-cells. 19 T-cell response to MI include both conventional and Foxp3 + regulatory CD4 + T-cell activation and proliferation in heart-draining lymph nodes. 20 The absolute number of Foxp3 + T-cells in lymph nodes and myocardium peaks on day 7, whereas their relative level remains nearly doubled until at least day 56.…”

Section: Myocardial Lymphocyte Subsets In Steadymentioning

confidence: 99%

Role of Lymphocytes in Myocardial Injury, Healing, and Remodeling After Myocardial Infarction

Hofmann

Frantz

2015

Circulation Research

231

177

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“…In patients with acute myocardial infarction (MI), high levels of the B‐cell specific cytokines, chemokine (C‐C motif) ligand 7 and B‐cell activating factor, predict increased risk of death and recurrent MI 21. In addition, hypertensive patients with high percentages of CD40 + B cells were at lower risk for stroke,22 whereas high numbers of CD86 + B cells showed higher risk for stroke 22.…”

Section: Introductionmentioning

confidence: 99%

High Levels of (Un)Switched Memory B Cells Are Associated With Better Outcome in Patients With Advanced Atherosclerotic Disease

Meeuwsen

Duijvenvoorde

Gohar

et al. 2017

JAHA

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BackgroundAtherosclerosis is an inflammatory lipid disorder and the main underlying pathology of acute ischemic events. Despite a vast amount of data from murine atherosclerosis models, evidence of B‐cell involvement in human atherosclerotic disease is limited. We therefore investigated the association of circulating B‐cell subtypes with the occurrence of secondary cardiovascular events in advanced atherosclerotic disease.Methods and ResultsThis cohort study consists of 168 patients who were included in the Athero‐Express biobank between 2009 and 2011. Before surgery, peripheral blood mononuclear cells were isolated and stored in liquid nitrogen. After gentle thawing of the peripheral blood mononuclear cells, different B‐cell subtypes including naïve, (un)switched memory, and CD27+ CD43+ B1‐like B cells, were analyzed by flow cytometry. Univariable and multivariable Cox proportional hazard models were used to analyze associations between B‐cell subtypes, circulating antibodies and secondary cardiovascular manifestations during the 3‐year follow‐up period. Mean age was 70.1±9.6 years, males represented 62.8% of the population, and 54 patients had secondary manifestations during follow‐up. High numbers of unswitched memory cells were protective against secondary outcome (hazard ratio, 0.30 [95% CI, 0.13–0.69]; P<0.01). Similar results were obtained for the switched memory cells that also showed to be protective against secondary outcome (hazard ratio, 0.33 [95% CI, 0.14–0.77]; P=0.01).ConclusionsA high number of (un)switched memory B cells is associated with better outcome following carotid artery endarterectomy. These findings suggest a potential role for B‐cell subsets in prediction and prevention of secondary cardiovascular events in patients with atherosclerosis.

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B lymphocytes trigger monocyte mobilization and impair heart function after acute myocardial infarction

Cited by 460 publications

References 44 publications

Splenic B Cells fromHymenolepis diminuta–Infected Mice Ameliorate Colitis Independent of T Cells and via Cooperation with Macrophages

Splenic B Cells fromHymenolepis diminuta–Infected Mice Ameliorate Colitis Independent of T Cells and via Cooperation with Macrophages

Role of Lymphocytes in Myocardial Injury, Healing, and Remodeling After Myocardial Infarction

High Levels of (Un)Switched Memory B Cells Are Associated With Better Outcome in Patients With Advanced Atherosclerotic Disease

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