IL-17, IL-22 and Their Producing Cells: Role in Inflammation by Franco Di Padova M.D., Bernhard Ryffel M.D., Valerie

By Franco Di Padova M.D., Bernhard Ryffel M.D., Valerie Quesniaux Ph.D. (auth.), Valérie Quesniaux, Bernhard Ryffel, Franco Padova (eds.)

The wisdom of Th17 cells and different mobile populations which secrete IL-17A, and/or IL-22 has improved greatly because the booklet of the 1st variation “Th17 Cells: function in irritation and Autoimmune affliction” in 2008. the current quantity has been thoroughly revised with the addition of latest chapters at the IL-17 receptor relatives and signaling, and an in-depth evaluate of IL-22 and innate lymphoid cells. The differentiation of naïve T cells into regulatory T cells and Th17 cells in addition to the plasticity of Th17 cells is mentioned. The function of IL-22 in cutaneous irritation together with psoriasis has been reviewed. additionally, the quantity includes severe updates on autoimmunity, organ transplantation, tumor immunology and genetic mouse types for mechanistic reports. finally, the most recent medical growth in neutralizing antibodies to IL-17A, IL-17RA not just confirms the healing promise foreseen in 2008, but additionally improves our wisdom of the pathogenesis of autoimmune illnesses. In precis, it is a well timed replace and critical evaluate of the scientific and experimental features of IL-17, IL-22 and their generating cells.

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Extra info for IL-17, IL-22 and Their Producing Cells: Role in Inflammation and Autoimmunity

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1007/978-3-0348-0522-3_3, # Springer Basel 2013 37 38 F. Shen with IL-17A among other IL-17-like cytokines. The crystal structure of IL-17F/F [10] and IL-17A/A [11] homodimers revealed a “cysteine knot”-like structure similar to nerve growth factor (NGF). IL-17A/F heterodimer was later identified from activated human and mouse CD4+ T cells [12, 13]. Although initially found in the adaptive immune system, IL-17A and IL-17F can also be produced by other innate immune cells in vivo [14]. Both of IL-17A and IL-17F are able to mount a strong inflammatory response and have quickly become major therapeutic targets under consideration for autoimmune diseases [15].

The impressive consequences of this IL-22 influence were demonstrated using a three-dimensional epidermis model: acanthosis (thickening of the epidermis), parakeratosis (retention of nuclei in the stratum corneum), and hypogranularity (loss of keratohyalin granules) [87, 102]. Interestingly, the influence of IL-22 on the keratinocyte differentiation is not shared by the Th1 and Th17 cell lead cytokines, whereas the latter also have a clear impact on antimicrobial protein (IFN-g, IL-17; see below) and MMP (IFN-g) expression [87].

Li J, Tomkinson KN, Tan XY, Wu P, Yan G, Spaulding V, Deng B, Annis-Freeman B, Heveron K, Zollner R et al (2004) Temporal associations between interleukin 22 and the extracellular domains of IL-22R and IL-10R2. Int Immunopharmacol 4:693–708 76. Wolk K, Witte E, Reineke U, Witte K, Friedrich M, Sterry W, Asadullah K, Volk HD, Sabat R (2005) Is there an interaction between interleukin-10 and interleukin-22? Genes Immun 6:8–18 77. Bleicher L, de Moura PR, Watanabe L, Colau D, Dumoutier L, Renauld JC, Polikarpov I (2008) Crystal structure of the IL-22/IL-22R1 complex and its implications for the IL-22 signaling mechanism.

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