Upregulation of Bcl-3 may trigger inflammatory
Upregulation of Bcl-3 may trigger inflammatory bowel disease
The inflammatory bowel diseases (IBDs), which mainly include ulcerative colitis (UC) and Crohn’s disease (CD), are characterized by chronic inflammation of the gastrointestinal tract. A lot of efforts have been made to elucidate the mechanism of IBD, but its pathogenesis is not completely understood.
Now a study led by scientists from from the University of Mainz, University Erlangen-Nürnberg, and several other institutions in Germany has revealed that increased expression of the protein Bcl-3 may result in inflammatory bowel disease (IBD). The study “Elevated levels of Bcl-3 inhibits Treg development and function resulting in spontaneous colitis” is published online in Nature Communications.
Bcl-3, or called B-cell lymphoma 3-encoded protein, is a protein that is encoded by the BCL3 gene. BCL3 is a proto-oncogene candidate and has been linked to a number of cancers, such as lymphoma. The protein Bcl-3 functions as a transcriptional coactivator.
The aim of this study is to determine whether Bcl-3 could have a role in the pathogenesis of human IBD. Study leader Nadine H velmeyer and colleagues and colleagues collected colonic tissue samples from people with or without IBD and used immunohistochemistry to examine Bcl-3 expression levels in these samples. Results showed that IBD patients had increased numbers of CD4+ T cells in their inflamed colon in comparison with control subjects, indicating that there is a strong association between Bcl-3-expressing CD4+ T cells and the pathogenesis of IBD.
Next, the researchers investigated mice with T-cell-specific overexpression of Bcl-3. Over time, these mice experienced severe diarrhoea and rectal prolapse, and spontaneously developed severe intestinal inflammation due to defective Treg cell development and function. Treg cells (Regulatory T cells) are known to help maintain gut immune homeostasis, and express the biomarkers CD4, FOXP3, and CD25. Additionally, previous studies have shown that defects in Treg cell function contribute to the development of IBD. Collectively, the study shows that Bcl-3 might be a trigger IBD, a common disease that affects millions of people worldwide. “Specifically targeting the activity of Bcl-3 in IBD may represent an effective strategy for the inhibition of gut inflammation,” the researchers concluded. (CusAb offers various proteins such as Recombinant AQP2 Bcl-3, CD4, FOXP3, and CD25.)
The inflammatory bowel diseases (IBDs), which mainly include ulcerative colitis (UC) and Crohn’s disease (CD), are characterized by chronic inflammation of the gastrointestinal tract. A lot of efforts have been made to elucidate the mechanism of IBD, but its pathogenesis is not completely understood.
Now a study led by scientists from from the University of Mainz, University Erlangen-Nürnberg, and several other institutions in Germany has revealed that increased expression of the protein Bcl-3 may result in inflammatory bowel disease (IBD). The study “Elevated levels of Bcl-3 inhibits Treg development and function resulting in spontaneous colitis” is published online in Nature Communications.
Bcl-3, or called B-cell lymphoma 3-encoded protein, is a protein that is encoded by the BCL3 gene. BCL3 is a proto-oncogene candidate and has been linked to a number of cancers, such as lymphoma. The protein Bcl-3 functions as a transcriptional coactivator.
The aim of this study is to determine whether Bcl-3 could have a role in the pathogenesis of human IBD. Study leader Nadine H velmeyer and colleagues and colleagues collected colonic tissue samples from people with or without IBD and used immunohistochemistry to examine Bcl-3 expression levels in these samples. Results showed that IBD patients had increased numbers of CD4+ T cells in their inflamed colon in comparison with control subjects, indicating that there is a strong association between Bcl-3-expressing CD4+ T cells and the pathogenesis of IBD.
Next, the researchers investigated mice with T-cell-specific overexpression of Bcl-3. Over time, these mice experienced severe diarrhoea and rectal prolapse, and spontaneously developed severe intestinal inflammation due to defective Treg cell development and function. Treg cells (Regulatory T cells) are known to help maintain gut immune homeostasis, and express the biomarkers CD4, FOXP3, and CD25. Additionally, previous studies have shown that defects in Treg cell function contribute to the development of IBD. Collectively, the study shows that Bcl-3 might be a trigger IBD, a common disease that affects millions of people worldwide. “Specifically targeting the activity of Bcl-3 in IBD may represent an effective strategy for the inhibition of gut inflammation,” the researchers concluded. (CusAb offers various proteins such as Recombinant AQP2 Bcl-3, CD4, FOXP3, and CD25.)
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