TNF-α-Secreting B Cells Contribute to Myocardial Fibrosis in Dilated Cardiomyopathy
Purpose Excessive inflammation responses mediated by $ CD4^{+} $ T cells contributes to myocardial fibrosis in dilated cardiomyopathy (DCM) resulting from viral myocarditis. Recently, some scholars discovered that B cells harbored an abnormal pro-inflammatory capacity besides the production of autoantibodies. Thus, we aimed to explore whether and which type of B cells act on myocardial fibrosis in DCM. Methods A total of 56 newly hospitalized DCM patients were studied, and among these, 17 patients accepted the gadolinium enhanced cardiovascular magnetic resonance imaging (MRI) for myocardial fibrosis evaluations. Results B cell functions including the frequency and proliferation were significantly elevated in DCM patients. After screening the important cytokines including IL-1β, IL-6, IL-10, IL-17, TNF-α and TGF-β produced in these B cells by flow cytometry, we found that only the TNF-α-secreting B cells were obviously increased. Furthermore, the TNF-α protein secretion and mRNA levels were also enhanced in LPS-stimulated B cell isolated from DCM patients. In addition, 10 patients (59 %) with increased TNF-α-secreting B cells showed late enhancement and boosted serum procollagen type III compared with the other 7 patients (41 %) whose enhancement could not be detected. Moreover, the frequencies of TNF-α-secreting B cells were negatively correlated with LVEF and positively correlated with LVEDD, NT-proBNP and procollagen type III in all of the DCM patients. Conclusions Our study firstly suggested that TNF-α-secreting B cells were involved in myocardial fibrosis, which revealed the new pathogenic mechanism of B cells in DCM, and therapeutic targets against these cells might be valuable..
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2013 |
|---|---|
| Erschienen: |
2013 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:33 |
|---|---|
| Enthalten in: |
Journal of clinical immunology - 33(2013), 5 vom: 05. Apr., Seite 1002-1008 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Yu, Miao [VerfasserIn] |
|---|
| Links: |
Volltext [lizenzpflichtig] |
|---|
| BKL: | |
|---|---|
| Themen: |
| doi: |
10.1007/s10875-013-9889-y |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
SPR014241951 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | SPR014241951 | ||
| 003 | DE-627 | ||
| 005 | 20230519230933.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 201006s2013 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1007/s10875-013-9889-y |2 doi | |
| 035 | |a (DE-627)SPR014241951 | ||
| 035 | |a (SPR)s10875-013-9889-y-e | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 082 | 0 | 4 | |a 610 |q ASE |
| 084 | |a 44.45 |2 bkl | ||
| 100 | 1 | |a Yu, Miao |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a TNF-α-Secreting B Cells Contribute to Myocardial Fibrosis in Dilated Cardiomyopathy |
| 264 | 1 | |c 2013 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a Computermedien |b c |2 rdamedia | ||
| 338 | |a Online-Ressource |b cr |2 rdacarrier | ||
| 520 | |a Purpose Excessive inflammation responses mediated by $ CD4^{+} $ T cells contributes to myocardial fibrosis in dilated cardiomyopathy (DCM) resulting from viral myocarditis. Recently, some scholars discovered that B cells harbored an abnormal pro-inflammatory capacity besides the production of autoantibodies. Thus, we aimed to explore whether and which type of B cells act on myocardial fibrosis in DCM. Methods A total of 56 newly hospitalized DCM patients were studied, and among these, 17 patients accepted the gadolinium enhanced cardiovascular magnetic resonance imaging (MRI) for myocardial fibrosis evaluations. Results B cell functions including the frequency and proliferation were significantly elevated in DCM patients. After screening the important cytokines including IL-1β, IL-6, IL-10, IL-17, TNF-α and TGF-β produced in these B cells by flow cytometry, we found that only the TNF-α-secreting B cells were obviously increased. Furthermore, the TNF-α protein secretion and mRNA levels were also enhanced in LPS-stimulated B cell isolated from DCM patients. In addition, 10 patients (59 %) with increased TNF-α-secreting B cells showed late enhancement and boosted serum procollagen type III compared with the other 7 patients (41 %) whose enhancement could not be detected. Moreover, the frequencies of TNF-α-secreting B cells were negatively correlated with LVEF and positively correlated with LVEDD, NT-proBNP and procollagen type III in all of the DCM patients. Conclusions Our study firstly suggested that TNF-α-secreting B cells were involved in myocardial fibrosis, which revealed the new pathogenic mechanism of B cells in DCM, and therapeutic targets against these cells might be valuable. | ||
| 650 | 4 | |a B cells |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a inflammation |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a TNF-α |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a myocardial fibrosis |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Wen, Shuang |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Min |e verfasserin |4 aut | |
| 700 | 1 | |a Liang, Wei |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Huan-Huan |e verfasserin |4 aut | |
| 700 | 1 | |a Long, Qi |e verfasserin |4 aut | |
| 700 | 1 | |a Guo, He-Ping |e verfasserin |4 aut | |
| 700 | 1 | |a Liao, Yu-Hua |e verfasserin |4 aut | |
| 700 | 1 | |a Yuan, Jing |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Journal of clinical immunology |d Dordrecht [u.a.] : Springer Science + Business Media B.V, 1981 |g 33(2013), 5 vom: 05. Apr., Seite 1002-1008 |w (DE-627)SPR014233401 |w (DE-600)2016755-6 |x 1573-2592 |7 nnns |
| 773 | 1 | 8 | |g volume:33 |g year:2013 |g number:5 |g day:05 |g month:04 |g pages:1002-1008 |
| 856 | 4 | 0 | |u https://dx.doi.org/10.1007/s10875-013-9889-y |z lizenzpflichtig |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_SPRINGER | ||
| 912 | |a SSG-OLC-PHA | ||
| 936 | b | k | |a 44.45 |q ASE |
| 951 | |a AR | ||
| 952 | |d 33 |j 2013 |e 5 |b 05 |c 04 |h 1002-1008 | ||