Regulation of Cytokine Gene Expression in Immunity and Diseases

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Dillon, S. Yeast zymosan, a stimulus for TLR2 and dectin-1, induces regulatory antigen-presenting cells and immunological tolerance.


  1. Regulation of Cytokine Gene Expression in Immunity and Diseases | SpringerLink?
  2. Tissue-specific Regulation of Cytokine Gene Expression.
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Diveu, C. Evans, J. Novel suppressive function of transitional 2 B cells in experimental arthritis. Feske, S. Calcium signalling in lymphocyte activation and disease. Fillatreau, S. B cells regulate autoimmunity by provision of IL Fiorentino, D. Two types of mouse T helper cell. Th2 clones secrete a factor that inhibits cytokine production by Th1 clones. IL acts on the antigen-presenting cell to inhibit cytokine production by Th1 cells. Fitzgerald, D. Suppression of autoimmune inflammation of the central nervous system by interleukin 10 secreted by interleukin stimulated T cells.

Franke, A. Gafa, V. Gascoyne, D. The basic leucine zipper transcription factor E4BP4 is essential for natural killer cell development. Gateva, V. Geurtsen, J. Identification of mycobacterial alpha-glucan as a novel ligand for DC-SIGN: involvement of mycobacterial capsular polysaccharides in host immune modulation. Glocker, E. Inflammatory bowel disease and mutations affecting the interleukin receptor. Grant, L. Genes Immun. Gray, M. Apoptotic cells protect mice from autoimmune inflammation by the induction of regulatory B cells. Gringhuis, S. Dectin-1 directs T helper cell differentiation by controlling noncanonical NF-kappaB activation through Raf-1 and Syk.

Groux, H. Nature , — Inoue, S. Inhibitory effects of B cells on antitumor immunity. Cancer Res. Jankovic, D. Jones, E. Kaiser, F. TPL-2 negatively regulates interferon-beta production in macrophages and myeloid dendritic cells. Kallies, A.

Cytokine - Wikipedia

Transcriptional repressor Blimp-1 is essential for T cell homeostasis and self-tolerance. Kamanaka, M. Expression of interleukin in intestinal lymphocytes detected by an interleukin reporter knockin tiger mouse. Immunity 25, — Kamizono, S. Kinnebrew, M. Immunity 36, — Kuhn, R. Interleukindeficient mice develop chronic enterocolitis. Cell 75, — Lampropoulou, V. TLR-activated B cells suppress T cell-mediated autoimmunity. Li, D. Lundy, S. Arthritis Res. Madan, R. Nonredundant roles for B cell-derived IL in immune counter-regulation.

Martins, G. Transcriptional repressor Blimp-1 regulates T cell homeostasis and function.

Bibliographic Information

Matsumoto, M. Immunity 34, — Mauri, C. Immune regulatory function of B cells. Prevention of arthritis by interleukin producing B cells. Therapeutic activity of agonistic monoclonal antibodies against CD40 in a chronic autoimmune inflammatory process. Maynard, C. Nat Immunol. McGeachy, M. Mizoguchi, A. Chronic intestinal inflammatory condition generates ILproducing regulatory B cell subset characterized by CD1d upregulation.

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Immunity 16, — Mizoguchi, E. Regulatory role of mature B cells in a murine model of inflammatory bowel disease. Mizuki, N. Motomura, Y. Neves, P. Signaling via the MyD88 adaptor protein in B cells suppresses protective immunity during Salmonella typhimurium infection. Immunity 33, — Nutt, S. Blimp-1 connects the intrinsic and extrinsic regulation of T cell homeostasis. O'Garra, A.

Ly-1 B B-1 cells are the main source of B cell-derived interleukin Pot, C. Remmers, E. Rogers, N. Syk-dependent cytokine induction by Dectin-1 reveals a novel pattern recognition pathway for C type lectins. Immunity 22, — Rubtsov, Y. Regulatory T cell-derived interleukin limits inflammation at environmental interfaces.

Immunity 28, — Saraiva, M. Identification of a macrophage-specific chromatin signature in the IL locus. Immunity 31, — The regulation of IL production by immune cells.

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Sato, T. Interleukin 10 production by human melanoma. Scapini, P. B cell-derived IL suppresses inflammatory disease in Lyn-deficient mice.


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  • Shaw, M. Shimomura, Y. Regulatory role of B-1 B cells in chronic colitis. Shoemaker, J. Stumhofer, J. Sun, J. Wang, Z. Regulation of IL gene expression in Th2 cells by Jun proteins. Wolf, S. Experimental autoimmune encephalomyelitis induction in genetically B cell-deficient mice. Xu, J. Yanaba, K.

    Zhou, Y. Ziegler-Heitbrock, L. Zielinski, C. Keywords: epigenetics, interleukin, plasticity, regulatory B cells, transcriptional regulation. This is an open-access article distributed under the terms of the Creative Commons Attribution License , which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc. Toggle navigation. Login Register Login using. However, the relationship between pro-inflammatory stimuli and glucocorticoids with respect to inducing DUSP1 expression is central to this outcome.

    The inductive effects of pro-inflammatory stimuli and the glucocorticoid summate, or synergize, to increase DUSP1 expression 35 , 38 — Regulatory loops controlling inflammatory gene expression. B , type I coherent and incoherent feedforward loops are depicted. In the type I coherent feedforward loop panel i , X positively regulates Y, and Z is positively regulated by both X and Y. In the type I incoherent feedforward loop panel ii , X positively regulates both Y and Z, but Y negatively regulates Z. Additional, glucocorticoid-induced effector processes are therefore likely to play additional repressive roles.

    Data from a ChIP-seq analysis by Kadiyala et al. Although overall GR occupancy at each gene locus was largely unaffected by TNF, site-specific differences are apparent. In the additional presence of dexamethasone, RELA binding is slightly reduced red arrow. However, although GR occupancy at this same region was not readily apparent with dexamethasone alone, with TNF plus dexamethasone, GR recruitment is induced red arrow. These regions did not show material RELA occupancy. This concept of feedback control in inflammation and enhancement, or maintenance, by glucocorticoid is likely to be relevant to multiple regulatory genes.

    A common regulatory circuit in the control of signal transduction and gene expression is the feedforward loop Such motifs are widespread in biological systems and apply to transcriptional regulation by nuclear hormone receptors In the simplest configuration, X and Y are positive regulators, for example, transcription factors, and the unit is described as a coherent feedforward loop Fig.

    Tissue-specific Regulation of Cytokine Gene Expression

    However, if Y were to negatively regulate Z, the effect of the two arms i. Thus, X leads to activation of Y and Z. However, increasing levels of the negative regulator, Y, progressively switch off Z and produces pulsed, or spike-like, dynamics for Z ZFP36 induction occurs in many cells, including A epithelial and primary human airway smooth muscle cells 61 , Thus, inflammatory mRNAs subject to control by MAPKs and ZFPdependent feedforward regulation reveal complex kinetics due to interplay between feedback and incoherent feedforward control.

    The above data produce various complications in the context of active glucocorticoid signaling. Conversely, in both in vivo inhaled glucocorticoid and cell culture, glucocorticoids alone up-regulate ZFP36 expression 16 , 72 — Furthermore, in the presence of pro-inflammatory stimulus plus glucocorticoid, the glucocorticoid-mediated loss of p38 MAPK activity may result in elevated levels of unphosphorylated ZFP36 that displays the greatest ARE-destabilizing activity Indeed, although this effect is described in airway smooth muscle cells 71 , a detailed analysis is required to confirm functionality.

    Nevertheless, simultaneous silencing of DUSP1 and ZFP36 in A cells revealed little effect on the dexamethasone-dependent repression of inflammatory mRNAs and suggests that other glucocorticoid-induced, or activated, effectors are important for repression Similarly, i. Thus, in vitro and in vivo , DUSP1 maintains expression of inflammatory genes! Indeed, mice lacking Irf1 are susceptible to death during viral infections 86 , whereas ubiquitin-mediated proteasomal degradation of IRF1 allows viral suppression of the immune response Such data are consistent with the phosphorylation and ubiquitination of IRF1 coupled with a half-life of just 30 min following induction by IL1B 77 , 88 , Loss of feedforward control may promote glucocorticoid resistance.

    This effect also occurs following MAPK inhibition. Therefore, the existence of additional mechanisms of repression must be invoked. B , data are modified from Shah et al. Although the generalizability of these data remains to be explored, we speculate that the maintenance of IRF1, as well as the coupled expression of key immune genes, for example CXCL10, is desirable during infections and could confer an advantage to the host Indeed, although glucocorticoids dampen inflammation to promote healing, their ability to maintain select immune responses may also represent a key function of GR.

    This implicates independent mechanisms of glucocorticoid repression that allow differential repression of IRF1-dependent genes Fig. Incoherent feedforward control by MAPK pathways is not without precedent. Likewise, the ubiquitin ligase, ITCH, is a substrate for JNK and promotes ubiquitination and proteolysis of signaling molecules and transcription factors necessary to activate pro-apoptotic gene expression Thus, the transcription of many genes is inhibited by MAPKs Furthermore, as suggested for IRF1 63 , the ability of glucocorticoids to induce DUSP1 expression and reduce MAPK activity should contribute toward maintaining, even enhancing, the expression of such genes.

    This concept is supported by the large number of LPS-induced transcripts that show reduced expression following knock-out of Dusp1 66 , Although we suggest a role in mediating resistance of CXCL10 to glucocorticoid treatment, the wider implication of genes that are negatively regulated by MAPKs is currently underappreciated. As discussed above, inflammatory signaling is subject to intense negative control that may be enhanced by glucocorticoids.

    Similarly, the effect of glucocorticoid stimulation alone on expression of any specific gene may reveal only weak induction, and such targets may thus appear unlikely to be important effectors of glucocorticoid action. However, integrated analysis of ChIP-seq and expression data can reveal patterns that suggest cooperation between GR and inflammatory transcription factors at specific enhancers Fig.

    These are therefore revealed as potentially glucocorticoid-regulated, despite an apparently minimal effect of glucocorticoid on expression of the associated gene. For example, SOD2, which protects against oxidative stress, is very weakly induced by glucocorticoid in airway epithelial cells, but when induced by IL1B, it is only modestly repressed Fig. Importantly, and probably more contentiously, we speculate that this effect may also extend to other, apparently pro-inflammatory, genes.

    Thus, other maintained genes Fig. Pro-inflammatory signals necessarily interact with GR signaling to maintain, or enhance, the expression of regulatory genes. Rather, many such regulators are specifically targeted by GR, enabling co-regulation and ensuring maintenance of expression in the context of glucocorticoid. Thus, cooperation between GR and inflammatory transcription factors allows GR transactivation to promote repression of inflammation.

    This raises the question as to the physical determinants of GR cooperation versus direct repression by GR. Certainly, differences in the nature and location of GR-binding sites relative to an inflammatory factor could play a role. Therapeutically, this cooperativity with GR to maintain, or induce, regulatory genes suggests a need for caution.


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    • When seeking to identify novel GR ligands with reduced side-effect profiles, simply screening for reduced GR transactivation may be quite unhelpful This makes biological sense in the context of feedback and feedforward control. Although SOD2 may be protective against oxidative injury, cytokines, such as IL32 or CSF3, may link to inflammatory responses that are maintained by the glucocorticoid. GR recruitment may, in the same way as the feedback regulator genes, actively maintain expression. This requires careful testing, but the identification of multiple genes with apparent effects on inflammation, proliferation, and cell migration that are all modestly glucocorticoid-induced in vivo raises the prospect that the maintenance by direct GR binding is widespread Maintenance of inflammatory gene expression may also be achieved by reducing feedforward control.

      This may be advantageous in the context of viral infections, but the maintained expression of such mediators may be undesirable in chronic inflammatory disease. This raises a radical line of thought. Certainly, reducing glucocorticoid-induced DUSP1 expression can have relatively little effect on inflammatory gene expression 31 , presumably due to other glucocorticoid-induced effectors providing redundant actions.

      Identification of inflammatory genes that evade repression also allows consideration of alternate strategies, for example small molecule inhibitors, to limit expression and would necessarily act as an add-on therapy alongside conventional GR-based approaches. Nevertheless, the above discussion highlights an urgent need for modeling and systems-based approaches to better predict the behavior of inflammatory pathways and gene expression.

      The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. Gerber, unpublished data. You'll be in good company.

      Journal of Lipid Research. Edited by Luke O'Neill. Previous Section Next Section. Figure 1. Figure 2. Figure 3. Reduced feedforward control promotes resistance to glucocorticoid As noted, glucocorticoids induce DUSP1 expression, down-regulate MAPK activity, and promote repression of inflammatory genes. Figure 4. Previous Section. Oakley , R. Allergy Clin. CrossRef Medline Google Scholar. Barnes , P. CrossRef Google Scholar. Keenan , C. Drug Discov. Today 17 , — Medline Google Scholar. Ammit , A. Sukkar , M. Lung Cell Mol. Zhang , N. Langlais , D. Busillo , J.

      Lannan , E. Endocrinology , — King , E. Trends Endocrinol. Rao , N. Genome Res. Kadiyala , V. Leigh , R. Google Scholar. Newton , R. Petta , I. Clark , A. Ito , K. Hua , G. Surjit , M. Cell , — Hudson , W. Biddie , S.