Users can feel how a part of the heavy chain of the antibody gets into the pocket of the receptor, and clamps the receptor in an inactive conformational state.This model can be separated into three parts to access the ligand-binding site.
The blood vasculature regulates both the development and function of secondary lymphoid organs by providing a portal for entry of haemopoietic cells. During the development of lymphoid organs in the embryo, blood vessels deliver lymphoid tissue inducer cells which initiate and sustain the development of lymphoid tissues. In adults, the blood vessels are structurally distinct from those in other organs due to the requirement for high levels of lymphocyte recruitment under non-inflammatory conditions. In lymph nodes and Peyer’s patches, high endothelial venules (HEV) especially adapted for lymphocyte trafficking form a spatially organised network of blood vessels which controls the both the type of lymphocyte and the site of entry into lymphoid tissues. Uniquely, HEV express vascular addressins which regulate lymphocyte entry into lymphoid organs and are, therefore, critical to the function of lymphoid organs. Recent studies have demonstrated important roles for CD11c+ dendritic cells in the induction, as well as the maintenance, of vascular addressin expression and, therefore, the function of HEV. Tertiary lymphoid organs (TLOs) are HEV containing, lymph node-like structures that develop inside organised tissues undergoing chronic immune-mediated inflammation. In autoimmune lesions, the development of TLOs is thought to exacerbate disease. In cancerous tissues, the development of HEV and TLOs is associated with improved patient outcomes in several cancers. Therefore, it is important to understand what drives the development of HEV and TLOs and how these structures contribute to pathology. In several human diseases and experimental animal models of chronic inflammation, there are some similarities between the development and function of HEVs in LN and TLOs. This review will summarise current knowledge of how haemopoietic cells with lymphoid tissue-inducing, HEV-inducing and HEV-maintaining properties are recruited from the bloodstream to induce the development and control the function of lymphoid organs.
Plasma cells (PCs) produce antibodies that mediate immunity after infection or vaccination. In contrast to PCs in the bone marrow, PCs in the gut have been considered short lived. In this study, we studied PC dynamics in the human small intestine by cell-turnover analysis in organ transplants and by retrospective cell birth dating measuring carbon-14 in genomic DNA. We identified three distinct PC subsets: a CD19+ PC subset was dynamically exchanged, whereas of two CD19− PC subsets, CD45+ PCs exhibited little and CD45− PCs no replacement and had a median age of 11 and 22 yr, respectively. Accumulation of CD45− PCs during ageing and the presence of rotavirus-specific clones entirely within the CD19− PC subsets support selection and maintenance of protective PCs for life in human intestine.
The mammalian immune system has evolved over many millennia to be best equipped to protect the host from pathogen infection. In many cases, host and pathogen have coevolved, each acquiring sophisticated ways of inducing or protecting from disease. Epstein-Barr virus (EBV) is a human herpes virus that infects >90% of individuals. Despite its ubiquity, infection by EBV is often subclinical; this invariably reflects the necessity of the virus to preserve its host, balanced with sophisticated host immune mechanisms that maintain viral latency. However, EBV infection can result in various, and often fatal, clinical sequelae, including fulminant infectious mononucleosis, hemophagocytic lymphohistiocytosis, lymphoproliferative disease, organomegaly, and/or malignancy. Such clinical outcomes are typically observed in immunosuppressed individuals, with the most extreme cases being Mendelian primary immunodeficiencies (PIDs). Although these conditions are rare, they have provided critical insight into the cellular, biochemical, and molecular requirements for robust and long-lasting immunity against EBV infection. Here, we review the virology of EBV, mechanisms underlying disease pathogenesis in PIDs, and developments in immune cell–mediated therapy to treat disorders associated with or induced by EBV infection.
En quoi consiste l’immunothérapie ? D’où vient cette technique ? Pourquoi dit-on que cette méthode est “révolutionnaire”, qu’elle propose un changement radical de point de vue dans la manière de considérer le cancer ?
In addition to physical barriers, neutrophils are considered a part of the first line of immune defense. They can be found in the bloodstream, with a lifespan of 6-8 hours, and in tissue, where they can last up to seven days. The mechanisms that neutrophils utilize for host defense are phagocytosis, degranulation, cytokine production and, the most recently described, neutrophil extracellular trap (NET) production. NETs are DNA structures released due to chromatin decondensation and spreading, and they thus occupy 3-5 times the volume of condensed chromatin. Several proteins adhere to NETs, including histones and over 30 components of primary and secondary granules, among them components with bactericidal activity such as elastase, myeloperoxidase, cathepsin G, lactoferrin, pentraxin 3, gelatinase, proteinase 3, LL-37, peptidoglycan-binding proteins and others with bactericidal activity able to destroy virulence factors. Three models for NETosis are known to date. a) Suicidal NETosis, with a duration of 2-4 hours, is the best described model. b) In vital NETosis with nuclear DNA release, neutrophils release NETs without exhibiting loss of nuclear or plasma membrane within 5-60 minutes, and it is independent of ROS and the Raf/MERK/ERK pathway. c). The final type is Vital NETosis with release of mitochondrial DNA that is dependent on ROS and produced after stimuli with GM-CSF and LPS. Recent research has revealed neutrophils as more sophisticated immune cells that are able to precisely regulate their granular enzymes release by ion fluxes and can release immunomodulatory cytokines and chemokines that interact with various components of the immune system. Therefore, they can play a key role in autoimmunity and in autoinflammatory and metabolic diseases. In this review, we intend to show the two roles played by neutrophils: as a first line of defense against microorganisms and as a contributor to the pathogenesis of various illnesses, such as autoimmune, autoinflammatory and metabolic diseases.
Auteur d’un récent ouvrage sur l’immunologie, Philippe Kourilsky, professeur émérite au Collège de France et ancien directeur de l’Institut Pasteur, évoque les succès, les échecs et les espoirs de cette discipline dont il est l’un des grands spécialistes mondiaux.
The notion of an “antibody” goes back to Paul Ehrlich, who coined the German term antikoper in 1891. He proposed the idea of a lock-and-key mechanism for the binding of antibody to antigen. However, no-one really understood how a set of rather identical looking antibodies could recognise thousands or even millions of different antigens. The answer lay in the three-dimensional structure of the antibody, revealed independently by Gerald Edelman at Rockefeller University in New York and Rodney Porter of Oxford University.
Combattre le cancer, non pas avec un traitement de chimiothérapie et de radiothérapie, mais en utilisant le système immunitaire du patient : les chercheurs fondent de grands espoirs dans cette approche, qui porte le nom d'immunothérapie du cancer.
Cancer immunotherapy involves targeting receptors and ligands of T-cells and tumor cells to amplify an immune response. By targeting these receptors and ligands, T-cell anti-cancer activity can be regulated. This blog the contribution of the receptors CD28 and CTLA-4 as well as their ligands CD80 and CD86 and their involvement in T-cell co-stimulation and activation or inhibition. Learn more with ProSci!
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