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<title cf:type="text"><![CDATA[Progress in Biochemistry and Biophysics -->Reviews and Monographs]]></title>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Progress in The Differentiation, Regulation and Function of Th17 Lineage]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20070817]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[As a new identified help T cell lineage different from Th1 and Th2 cells, Th17 cell has been found played important roles in the pathogenesis of autoimmunity and inflammatory disease. To further identify their roles, the differentiation and regulation of Th17 cells has been widely explored recently. Now it has been confirmed that TGF-beta, combined with IL-6 or IL-21, play critical roles in the differentiation of Th17 cells. While IL-23 mainly contribute in promoting the secretion of IL-17 and maintaining the function of Th17 cells. Corresponding with the Th1,Th2, and Treg cells, which has special transcription factors T-bet、GATA3、Foxp3 respectively, now it has been confirmed that ROR-γt(retinoid-related orphan receptors-γt) is the special transcription factor which specially regulate the differentiation of Th17 cells. Th17 cells function through their secreted pro-inflammatory cytokines, including IL-17A, IL-17F, IL-21, IL-22, IL-6, TNF-α. Among them IL-21，which act as a autocrine cytokine of Th17 cells, play critical roles in promoting the differentiation of Th17 cells while inhibiting the differentiation and function of Th1 and Treg cells. On the other hand, IL-2, which is obligatory for the growth of Th1,Th2,Treg and CD8<sup>+</sup>T cells, now has been found negatively regulate the differentiation of Th17 cells. In all, differentiation of Th17 and Treg,Th1 cells are exactly regulated <i>in vivo</i>, in which TGF-beta played critical roles. As both Th1 and Th17 cells participate in the pathogenesis of autoimmunity and inflammatory diseases, are they play synergistic roles or function at different time point or location? How TGF-β regulate Th17 and Treg cells？Can Th17 cells be used as a target for immune tolerance induction? All above questions will certainly be of continuing interest.]]></description>
<pubDate>2008/2/18 0:00:00</pubDate>
<category><![CDATA[Reviews and Monographs]]></category>
<author><![CDATA[HAN Gen-Cheng and SHEN Bei-Fen]]></author>
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<atom:name>HAN Gen-Cheng and SHEN Bei-Fen</atom:name>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Recognition and Interaction of Innate Immune Receptors]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20070816]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[NKR and TLR are most important receptor superfamilies in innate immunity and act as first line of host defense against infection. Those receptors exert peculiar recognition mechanisms to sense danger signals and distinguish infectious nonself from noninfectious self. More importantly, they coordinate and regulate each other and therefore play major roles in initiation of innate immunity and also help to direct adaptive immune responses. The importance of recognition and interaction of those receptors are highlighted. The precise mechanisms can be harnessed to aid the rational design of therapy against infection, inflammation, cancer or autoimmune diseases.]]></description>
<pubDate>2008/2/18 0:00:00</pubDate>
<category><![CDATA[Reviews and Monographs]]></category>
<author><![CDATA[ZHANG Cai and TIAN Zhi-Gang]]></author>
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<atom:name>ZHANG Cai and TIAN Zhi-Gang</atom:name>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[T Cells Regulate Initial Inflammatory Responses During Acute Infection]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20080105]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Inflammation is a basic way in which the body reacts to infection, irritation or other injury. The key clinical feature of inflammation is redness, warmth, swelling and pain. A series of immune cells and cytokines are involved in the complicated and interrelated events during inflammation to work together to defend the body. Innate immune cells, including phagocytes, NK cells and dentritic cells, are the main effector cells in initiating an inflammatory response. Adaptive immune cells, for example, T cells which take part in the battle at the later phase of an inflammatory response could also temper the initial inflammatory responses during acute infection. On one hand, hosts rely on inflammatory responses to eliminate the pathogen, control the infection within the local site, and induce the adaptive immune response. However, on the other hand, over-reactive and chronic inflammation can also lead to some diseases. Consequently, the study of the mechanism of inflammation might lead to new treatment for patients with inflammation-related diseases.]]></description>
<pubDate>2008/2/19 0:00:00</pubDate>
<category><![CDATA[Reviews and Monographs]]></category>
<author><![CDATA[ZHAO Jie,YANG Xuan-Ming,DU Pei-Shuang and TANG Hong]]></author>
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<atom:name>ZHAO Jie,YANG Xuan-Ming,DU Pei-Shuang and TANG Hong</atom:name>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Progress in Epigenetic Regulation of V(D)J Recombination]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20080046]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[During lymphocyte development antigen receptor genes undergo V(D)J recombination to obtain antigen binding specificity and diversity. This process is not only controlled by genetic factors, such as tissue- and stage- specificity of RAG-1/2 protein, germline transcriptional activity and ACEs, but also regulated at epigenetic level. The chromatin accessibility of recombinase is associated with the chromatin configuration around the targeted gene segments. Thus, activation of V(D)J recombination requires the recruitment of remodeling complexes for changing the accessibility in the localized chromatin. Moreover, docking of remodeling complexes, which serve for creating active chromatin environment, relies on certain patterns of chromatin modification. Some recent findings regarding epigenetic regulation mechanisms in V(D)J recombination, such as CpG methylation, histone modification, nucleosome remodeling and nuclear topology were reviewed.]]></description>
<pubDate>2008/2/18 0:00:00</pubDate>
<category><![CDATA[Reviews and Monographs]]></category>
<author><![CDATA[ZHENG Chao-Gu and YAN Xi-Yun]]></author>
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<atom:name>ZHENG Chao-Gu and YAN Xi-Yun</atom:name>
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