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• W4205521334 abstract "European Journal of ImmunologyVolume 39, Issue 4 p. 919-920 In this issueFree Access In this issue First published: 06 April 2009 https://doi.org/10.1002/eji.200990019AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinked InRedditWechat Abstract Cover image The cover image, provided by Ghumra et al. (pp. 1147–1156), shows two views of a molecular model of human dimeric IgA1 revealing residues predicted to be critical for interaction with human Fcα/μR, a receptor with specificity for the Fc regions of IgA and IgM. The IgA heavy chains (tailpieces omitted) are shown in yellow, and the light chains in blue. The heavy chain residues proline 440 to phenylalanine 443 on the Cα3 domain of the IgA Fc region, implicated in hFcα/μR interaction, are shown as red spheres. The J (joining) chain of the dimeric IgA is not included in the model, but the white dotted line in the lower view indicates a possible position. Prolactin promotes Th17-mediated skin inflammation pp. 996–1006 Psoriasis vulgaris is an autoimmune dermatosis characterized by alterations in several immune-parameters. Some changes include an abundance of Th17 cell infiltration, as well as prolactin and CCL20 dysregulation. In this issue, Kanda et al. demonstrate that these are not independent events but are in fact intimately linked. The authors show that prolactin increases epidermal keratinocytes CCL20 production both alone and in synergy with IL-17. CCL20 production induced by prolactin was mediated via the activation of AP-1 and NF-κB through the MEK/ERK and JNK pathways; CCL20 in turn recruits Th17 cells via CCR6. Understanding the various components of this inflammatory loop may provide novel therapeutic targets for the treatment of psoriasis. Synergy between innate and adaptive immunity drives Schistosome-mediated prevention of autoimmune diabetes pp. 1098–1107 Although it is known that the soluble extract of Schistosoma mansoni eggs (SEA) prevents autoimmune diabetes in NOD mice, the mechanism of action remains unclear. In this issue, Zaccone et al. show that Foxp3+ Treg increase in the pancreas following SEA treatment of NOD mice. Furthermore, SEA has direct effects on both DC and T cells. On DC, SEA upregulates IL-2 and IL-10 secretion, and also upregulates C-type lectin receptors. In the absence of antigen presenting cells, SEA upregulates TGF-β and galectins on CD4+ T cells, and induces Foxp3+CD4+ T cells in a TGF-β-dependent fashion. In the context of type 1 diabetes inhibition by SEA, it appears that early expansion of Treg is an important event for immunomodulation and diabetes prevention. Therapeutic Treg: two key requirements pp. 1108–1117 Harnessing the powerful immunoregulatory properties of Foxp3+ Treg is the Holy Grail for many immunologists. In this issue, Stephens et al. have tested the requirements for Treg-mediated immunosuppression using the commonly used mouse model of multiple sclerosis, EAE. Transfer of Treg prior to immunization could completely prevent EAE development. Moreover, transfer of Treg in low numbers after disease onset could reverse progression of the chronic phase of disease, i.e. cure the disease. In both settings, the Treg's effects were conditional upon recognition of myelin autoantigen; polyclonal Treg were completely ineffective, indicating that translation to the clinic will require knowledge of the disease-relevant autoantigens recognized by Treg. Furthermore, CD4+CD25+ Treg could be divided into CD62Llo and CD62Lhi subsets, with the latter giving the best protection against EAE. This was attributed to a loss of Foxp3 expression by the CD62Llo subset after transfer. The CD62Lhi population maintained Foxp3 expression, but lost CD25 upon in vivo activation. The study suggests two key requirements for successful use of Treg in the clinic: identification of the autoantigen and the development of a new method of Treg purification that is independent of CD25. IL-10 fails to block Th17 memory pp. 1066–1077 The anti-inflammatory cytokine IL-10 is known to inhibit the induction of a wide range of pro-inflammatory mediators. Therefore, it has been tested with big expectations as a therapeutic in diseases associated with chronic inflammation. Clinical trials, however, remained largely disappointing and the reasons for this failure are not fully understood. In this issue, Naundorf et al. give an interesting new view to this story by studying the effects of IL-10 on established T-cell memory responses. Although IL-10 is able to inhibit directly the TCR-induced production of IFN-γ, an important effector cytokine in acute inflammation, it is not able to block IL-17 production from memory T cells despite an intact signal transduction. Adaptive epitopes: T cells adapt to epitopes, but how about vice versa? pp. 1056–1065 The T-cell epitope repertoire is composed of a limited number of short peptides properly processed and bound to MHC molecules. This small number of epitopes (approximately one to three per protein per allele on average) shapes the adaptive immune response. A comprehensive bioinformatic analysis shows that the CTL epitope repertoire may have evolved to optimize the immune response. In this issue, Almani et al. present a new epitope density measure, based on the combination of bioinformatic algorithms and named this the Size of Immune Repertoire (SIR) score. The SIR score distribution shows that the average epitope density of a protein is correlated with its importance/usefulness for immune selection. The SIR score is positively correlated with the RNA expression level, expression in the thymus and role in innate immune system. The selection of epitopes through evolution can be observed in the fraction of non-synonymous single nucleotide polymorphisms, which is higher inside epitopes than outside epitopes. Volume39, Issue4April 2009Pages 919-920 RelatedInformation" @default.
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