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Molecular mechanisms regulating NLRP3 inflammasome activation
Jo, Eun-Kyeong,Kim, Jin Kyung,Shin, Dong-Min,Sasakawa, Chihiro CHINESE SOCIETY OF IMMUNOLOGY 2016 CELLULAR AND MOLECULAR IMMUNOLOGY Vol.13 No.2
<P>Inflammasomes are multi-protein signaling complexes that trigger the activation of inflammatory caspases and the maturation of interleukin-1 beta. Among various inflammasome complexes, the NLRP3 inflammasome is best characterized and has been linked with various human autoinflammatory and autoimmune diseases. Thus, the NLRP3 inflammasome may be a promising target for anti-inflammatory therapies. In this review, we summarize the current understanding of the mechanisms by which the NLRP3 inflammasome is activated in the cytosol. We also describe the binding partners of NLRP3 inflammasome complexes activating or inhibiting the inflammasome assembly. Our knowledge of the mechanisms regulating NLRP3 inflammasome signaling and how these influence inflammatory responses offers further insight into potential therapeutic strategies to treat inflammatory diseases associated with dysregulation of the NLRP3 inflammasome.</P>
Retinoic acid enhances lactoferrin-induced IgA responses by increasing betaglycan expression
Lee, Jeong-Min,Jang, Young-Saeng,Jin, Bo-Ra,Kim, Sun-Jin,Kim, Hyeon-Jin,Kwon, Bo-Eun,Ko, Hyun-Jeong,Yoon, Sung-il,Lee, Geun-Shik,Kim, Woan-Sub,Seo, Goo-Young,Kim, Pyeung-Hyeun CHINESE SOCIETY OF IMMUNOLOGY 2016 CELLULAR AND MOLECULAR IMMUNOLOGY Vol.13 No.6
<P>Lactoferrin (LF) and retinoic acid (RA) are enriched in colostrum, milk, and mucosal tissues. We recently showed that LF-induced IgA class switching through binding to betaglycan (transforming growth factor-beta receptor III, T beta RIII) and activation of canonical TGF-beta signaling. We investigated the combined effect of LF and RA on the overall IgA response. An increase in IgA production by LF was further augmented by RA. This combination effect was also evident in Ig germ-line alpha (GL alpha) transcription and GLa promoter activity, indicating that LF in cooperation with RA increased IgA isotype switching. We subsequently found that RA enhanced T beta RIII expression and that this increase contributed to LF-stimulated IgA production. In addition to the IgA response, LF and RA in combination also enhanced the expression of the gut-homing molecules C-C chemokine receptor 9 (CCR9) and alpha 4 beta 7 on B cells. Finally, peroral administration of LF and RA enhanced the frequency of CCR9(+)IgA(+) plasma cells in the lamina propria. Taken together, these results suggest that LF in cooperation with RA can contribute to the establishment of gut IgA responses.</P>
Transcription factor IRF8 controls Th1-like regulatory T-cell function
Lee, Wonyong,Kim, Hyeong Su,Baek, Song Yi,Lee, Gap Ryol CHINESE SOCIETY OF IMMUNOLOGY 2016 CELLULAR AND MOLECULAR IMMUNOLOGY Vol.13 No.6
<P>Recent studies have suggested that regulatory T (Treg) cells comprise a heterogeneous population that regulates various aspects of the immune response, and that Treg cells use the factors that are expressed in their target cells to regulate them. We searched for factors that regulate Th1 response in Treg cells using a meta-analysis. In the process, we discovered that transcription factor interferon regulatory factor 8 (IRF8) was selectively expressed in Treg and Th1 cells. IRF8-deficient Treg cells showed defective expression of CXCR3 and aberrant expression of the II4 and II17 genes. Upon treatment with alpha galactosyl-C18-ceramide (alpha Gal-C18-Cer), IRF8-deficient mice showed defective Treg cell recruitment in the liver. Eliciting Th1 immune response by anti-CD40 antibody injection in mice induced IRF8 expression in Treg cells. The expression of IRF8 was induced by Foxp3 in Treg cells. IRF8 had no effect on T-bet expression in Treg and vice versa. Thus, our results strongly suggest that IRF8 controls Th1 immune response in Treg cells independent of T-bet.</P>
Diverse functions of VDUP1 in cell proliferation, differentiation, and diseases.
Kim, Sang Yong,Suh, Hyun-Woo,Chung, Jin Woong,Yoon, Suk-Ran,Choi, Inpyo CHINESE SOCIETY OF IMMUNOLOGY 2007 CELLULAR AND MOLECULAR IMMUNOLOGY Vol.4 No.5
<P>Vitamin D3 up-regulated protein 1 (VDUP1) is a multifunctional protein involved in maintaining cellular homeostasis. VDUP1 is induced by a variety of stresses. Inversely, VDUP1 is often reduced in various tumor tissues and cell lines. Over-expression of VDUP1 inhibits cell proliferation through cell cycle arrest. VDUP1 interacts with thioredoxin (Trx) and negatively regulates the expression and antioxidant function of Trx which is involved in redox regulation. VDUP1-/- mice are more susceptible to carcinogenesis than wild-type mice and are defective in establishing immune system including the development and function of natural killer cells. Furthermore, VDUP1-/- mice show impaired Kreb cycle-mediated fatty acid utilization. In this review, we have discussed the multifunctional roles of VDUP1 in diverse cellular responses, in particular its relation to proliferation, apoptosis, differentiation, and diseases such as cancer and stress-related diseases.</P>