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Self Tolerance --- Adaptive Immunity. --- Immunity, Innate. --- immunology.

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The Nod-like receptor (NLR) family of proteins are evolutionary conserved molecules that in plants and mammals have been implicated in innate immune sensing of microbes and infection-associated physiological changes, contributing to immune protection of the challenged host organism through the instruction of inflammatory responses, antimicrobial defense and adaptive immunity. Recent data however suggests that the biological roles of NLR go beyond the function of classical pattern recognition molecules (PRM) as they have been implicated in essential cellular processes including autophagy, apoptosis, modification of signal transduction and gene transcription as well as reproductive biology. In this research topic, we aim to provide a comprehensive state-of the art overview of the emerging functions of NLR in plant and mammalian immunity, cell biology and reproductive biology. Potential topics may include, but are not limited to the following areas: • Functions of NLRs as PRMs in infection • Cross-talk of NLRs with other PRMs • Signal transduction pathways of NLRs • New functions of NLRs other than pattern recognition • Structural aspects of NLR activation • Mechanisms of NLRs in cell biological processes • Aspects of NLRs in reproductive biology • Functions of NLRs in plant immune responses

Adaptive Immunity --- PAMP --- pathogens --- MAMP --- innate immunity --- Bacteria --- Sensing --- virus --- LRR --- DAMP --- Adaptive Immunity --- PAMP --- pathogens --- MAMP --- innate immunity --- Bacteria --- Sensing --- virus --- LRR --- DAMP

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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact

Medicine --- Immunology --- immune evolution --- innate immunity --- adaptive immunity --- host-microbe --- co-option --- immune evolution --- innate immunity --- adaptive immunity --- host-microbe --- co-option

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The immune system is central to human health and the focus of much medical research. Growing understanding of the immune system, and especially the creation of immune memory (long lasting protection), which can be harnessed in the design of vaccines, have been major breakthroughs in medicine.In this Very Short Introduction, Paul Klenerman describes the immune system, and how it works in health and disease. In particular he focuses on the human immune system, considering how it evolved, the basic rules that govern its behaviour, and the major health threats where it is important. The immune system comprises a series of organs, cells and chemical messengers which work together as a team to provide defence against infection. Klenerman discusses these components, the critical signals that trigger them and how they exert their protective effects, including so-called <"innate>" immune responses, which react very fast to infection, and <"adaptive>" immune responses, which have huge diversity and a capacity to recognise and defend against a massive array of micro-organisms. Klenerman also considers what happens when our immune systems fail to be activated effectively, leading to serious infections, problems with inherited diseases, and also HIV/AIDS. At the opposite extreme, as Klenerman shows, an over-exaggerated immune response leads to inflammatory diseases such as Multiple Sclerosis and Rheumatoid Arthritis, as well as allergy and asthma . Finally he looks at the <"Immune system v2.o>" - how immune therapies and vaccines can be advanced to protect us against the major diseases of the 21st century.

Immune system --- Immuunsysteem --- Adaptive Immunity --- Immune System Diseases --- Immune System --- immunology --- Immune System - immunology

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IL-22 is a cytokine mainly produced by a T cell subset named Th17.IL-22 acts on a receptor can also bind other cytokines similar to IL-22, namely IL-20 and IL-24. IL-22 appears to be involved in various inflammatory diseases such as colitis, where it plays an anti-inflammatory role and arthritis, where it plays a pro-inflammatory role.
Here, we studied the role of IL-22 and its receptor in an animal model of psoriasis, a chronic inflammatory disease wich is T (Th17) cell-dependent. To perform this study, we used the imiquimod-induced psoriasis-like skin inflammatory model. Imiquimod binds TLR7 and TLR8 and activates NFkB pathway causing inflammation. We applied the model to Wild Type (WT), IL-22 deficient or IL-22R deficient mice. These IL-22R deficient mice allow us to study not only the role of IL-22, but also the role of IL-20 and IL-24. IL-22-/- and IL-22R-/- mice seem to be protected in comparison with WT mice. Indeed, we observed an increase in skin redness and scaly plaques in WT mice treated with imiquimod versus IL-22-/- or IL-22R-/- mice that received the same treatment. We analysed gene expression in the skin of imiquimod-treated mice using microarray techniques. On the one hand, we observed an increased expression of inflammation markers and keratinocytes proliferation markers such as chemokines and keratin 14, on the other hand, a decreased expression of keratinocytes differentiation markers, such as loricrin. In contrast, IL-22-/- and IL-22R-/- mice treated with imiquimod showed a weaker variation of these genes as compared to WT mice. Moreover, injection of IL-22 neutralizing antibodies in WT mice conferred a similar protection to that observed in IL-22-/- mice, confirming the pathogenic role of IL-22 by applying our model to Rag2-/- or Rag2-/- IL-22-/- mice transferred or not with T cells. The results of this experiment suggest that IL-22 is produced predominantly by innate immune cells and that this production depends on the presence of T lymphocytes.
In conclusion, we have demonstrated that IL-22 plays a deleterious role in an experimental model of psoriasis in which innate immune cells represent the main source of this cytokine L’IL-22 est une cytokine produite majoritairement par une sous-population de lymphocytes T, les Th17. Elle agit sur un récepteur, l’IL-22R, exprimé au niveau de certains organes tels que le foie, les poumons, la peau et l’intestin. Ce récepteur peut également fixer d’autres cytokines ressemblant à l’IL-22, à savoir l’IL-20 et l’IL-24. L’IL-22 semble impliquée dans différentes maladies inflammatoires comme la colite où elle joue un rôle anti inflammatoire et l’arthrite où son rôle est pro-inflammatoire.
Au cours de ce mémoire, nous avons étudié le rôle de l’IL-22 et de son récepteur dans un modèle expérimental de psoriasis, une maladie inflammatoire chronique dépendante des lymphocytes T et plus particulièrement des lymphocytes Th17. Pour cela, nous avons utilisé le modèle de psoriasis induit par l’application cutanée d’imiquimod. L’imiquimod se fixe sur TLR7 et TLR8 et active le foie NFkB provoquant l’inflammation. Nous avons appliqué le modèle à des souris Wild Type (WT), déficientes en IL-22 ou déficientes en IL-22R. Ces dernières nos permettent d’étudier non seulement le rôle de l’IL-22R. Ces dernières nous permettent d’étudier non seulement le rôle de l’IL-22 mais également celui de l’IL-20 et de l’IL-24. Les souris IL-22-/- et IL-22R-/- semblent être protégées par rapport aux souris WT. En effet, nous observons, chez les souris WT traitées avec l’imiquimod, une rougeur de la peau et une desquamation plus importante que chez les souris IL-22-/- ou IL-22R-/- ayant reçu le même traitement. Nous avons analysé, par microarray, l’expression des gènes au niveau de la peau en réponse à l’émiquimod. Nous observons, d’une part, une augmentation de l’expression de gènes marqueurs d’inflammation et de prolifération des kératinocytes tels que les chémokines et la kératine 14, d’autre part, une diminution des gènes marqueurs de la différenciation des kératinocytes, tels que la loricrine. En revanche les souris IL-22-/- ou IL-22R-/- traitées à l’imiquimod présentent une variation moins forte de ces différents gènes par rapport aux souris WT. De plus, l’injection d’anticorps bloquant l’IL-22, attestant du rôle néfaste de l’IL-22 dans le psoriasis. En outre, nous avons tenté de déterminer si les lymphocytes T étaient la source principale d’IL-22 en appliquant notre modèle à des souris Rag2-/- ou Rag2-/- IL-22-/- transférées ou non avec des lymphocytes T. Cette expérience suggère que l’IL-22 est produite majoritairement par ces cellules du système immunitaire inné et que cette production dépend de la présence de lymphocytes T.
En conclusion, nous avons donc pu démontrer que l’IL-22 joue un rôle délétère dans ce modèle expérimental de psoriasis et que les cellules du système immunitaire inné en représentent la source principale

interleukin-22 --- Interleukin-22 receptor --- Psoriasis --- Cytokines --- Adaptive Immunity --- Immunity, Innate