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Our understanding of the human immune system has largely stemmed from studies with
Gilbert C FAURE's insight:
Great data! Have been convinced of that for a long time without support... any information about HLA diversity in various tissues?
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PLoS One. 2016 Mar 8;11(3):e0150677. doi: 10.1371/journal.pone.0150677. eCollection 2016. Research Support, Non-U.S. Gov't
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During the development of natural killer (NK) cells, activating receptor signaling drives the acquisition of inhibitory receptors during development, leading to the creation of a diverse pool of ligand-specific NK cells.
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Immunol Lett. 2016 Jul 30. pii: S0165-2478(16)30130-4. doi: 10.1016/j.imlet.2016.07.015. [Epub ahead of print]
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Thanks to the memory capabilities of our immune cells, our body knows how to fight pathogens better the second, third, and fourth times we encounter them.
Gilbert C FAURE's insight:
bis?
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News from JAMA — New Insights Into Arbovirus Infection and Immunity
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Publication date: 28 July 2016
Source:Cell, Volume 166, Issue 3 Author(s): Andrea J. Wolf, Christopher N. Reyes, Wenbin Liang, Courtney Becker, Kenichi Shimada, Matthew L. Wheeler, Hee Cheol Cho, Narcis I.
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The immune system is usually equipped to handle most bacterial infections, but certain cases of severe infection can leave a person extremely vulnerable wh
Via Krishan Maggon
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The powerful Immune synapse of the killer T cell is similar in many ways to the primary cilium and the spindles that orchestrate cell division
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Therapies that target and eliminate B cells have had some success in patients with autoimmune diseases such as systemic lupus erythematosus or rheumatoid arthritis. However, restoring tolerance in self-reactive B cells that lead to disease remains an unmet goal. The 1858T allele of protein tyrosine phosphatase nonreceptor type 22 (PTPN22 T) has been associated with autoreactive B cells in autoimmune disease in humans. Now, Schickel et al. report that this allele interferes with the development of central B cell tolerance in a humanized mouse model of autoimmunity and that blocking PTPN22 can restore this defect. If these observations hold true in humans, targeting PTPN22 may be able to restore B cell tolerance in patients with autoimmune disease.
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Meet us in D.C.! Find the latest developments in your field Hear lectures by the world’s foremost immunologists and poster presentations by scientists at every career stage Network with colleagues from more than 40 countries, and See the newest tools and techniques to benefit your research!
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Accumulating studies demonstrate that IL-21 modulates the differentiation of various CD4 and CD8 T cell subsets and provide insights into the underlying cellular and molecular processes that are influenced by this cytokine. Intriguingly, the effects of IL-21 on T cells can be complex and vary depending on the experimental system used. We review our current understanding of the roles of IL-21 in the generation of phenotypically distinct CD4 and CD8 T cell populations and discuss the potential environmental cues, cellular factors, and molecular mediators that impact the actions of IL-21. We propose that IL-21 acts in a context-dependent manner to accentuate T cell subset development.
Via Krishan Maggon
Krishan Maggon 's curator insight,
August 1, 2016 3:15 AM
Volume 37, Issue 8, p557–568, August 2016
Yuan Tian, Allan J. Zajac |
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Immunology and Cell Biology focuses on the general functioning of the immune system in its broadest sense, with a particular emphasis on its cell biology. Areas that are covered include but are not limited to: Cellular immunology, Innate and adaptive immunity, Immune responses to pathogens,Tumour immunology,Immunopathology, Immunotherapy, Immunogenetics, Immunological studies in humans and model organisms (including mouse, rat, Drosophila etc)
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Boss and colleagues provide mechanistic insight into cell-division-coupled transcriptional and epigenetic reprogramming events during plasma cell differentiation.
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In the study of cell signaling, one well established paradigm is that receptors on the surface of cells receive input from chemicals outside the cell such
Gilbert C FAURE's insight:
GPCR on wikipedia, not bad https://en.wikipedia.org/wiki/G_protein%E2%80%93coupled_receptor
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The response of a cell to ligands that activate cell surface receptors depends on the resulting protein-protein interactions that occur. The formation of different protein complexes leads to the activation of different intracellular signaling pathways and different cellular outputs. Thus, knowing which protein-protein interactions occur can be clinically important. To analyze these complexes in patient samples, Smith et al . devised a multiplex, antibody-based method and used it to capture complexes from T cell lysates and identify binding partners by flow cytometry. Mathematical analyses of these data enabled the construction of protein-protein interaction networks and revealed the relative abundances of particular complexes between resting and stimulated cells. Application of this technique to T cells from skin biopsies identified protein complexes that differed in their relative abundance between control donors and patients with an autoimmune skin disease. This type of analysis brings basic research a step closer to personalized therapy and may be useful as a diagnostic tool.
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J Immunol. 2016 Aug 1. pii: 1600526. [Epub ahead of print]
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Sci Rep. 2016 Aug 2;6:30004. doi: 10.1038/srep30004.
Gilbert C FAURE's insight:
don't forget teleosts
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A new study, led by scientists at The Scripps Research Institute, reveals a surprising twist in immune biology.
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Frontiers in Immunology, launched in 2010, has just received its first official Impact Factor of 5.695. In just 5 years, it has become the largest and the most cited open-access journal in Immunology, and the 7th most cited amongst all journals in Immunology. Impact Factor (IF), defined as the total number of citations in a given…
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Gilbert C FAURE's insight:
it was 2004, but still valid
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It takes no more than 100 seconds for the body’s immune cells to identify and kill a cancer cell.
Gilbert C FAURE's insight:
ça fait longtemps qu'on le dit
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Author Summary Mycobacterium tuberculosis ( Mtb ), the causative agent of human tuberculosis, is one of the most widely spread human pathogens, responsible for more than 9.6 million of new tuberculosis cases and 1.5 million deaths, annually.
Gilbert C FAURE's insight:
Abstract Mycobacterium tuberculosis (Mtb), possesses at least three type VII secretion systems, ESX-1, -3 and -5 that are actively involved in pathogenesis and host-pathogen interaction. We recently showed that an attenuated Mtb vaccine candidate (Mtb Δppe25-pe19), which lacks the characteristic ESX-5-associated pe/ppe genes, but harbors all other components of the ESX-5 system, induces CD4+ T-cell immune responses against non-esx-5-associated PE/PPE protein homologs. These T cells strongly cross-recognize the missing esx-5-associated PE/PPE proteins. Here, we characterized the fine composition of the functional cross-reactive Th1 effector subsets specific to the shared PE/PPE epitopes in mice immunized with the Mtb Δppe25-pe19 vaccine candidate. We provide evidence that the Mtb Δppe25-pe19 strain, despite its significant attenuation, is comparable to the WT Mtb strain with regard to: (i) its antigenic repertoire related to the different ESX systems, (ii) the induced Th1 effector subset composition, (iii) the differentiation status of the Th1 cells induced, and (iv) its particular features at stimulating the innate immune response. Indeed, we found significant contribution of PE/PPE-specific Th1 effector cells in the protective immunity against pulmonary Mtb infection. These results offer detailed insights into the immune mechanisms underlying the remarkable protective efficacy of the live attenuated Mtb Δppe25-pe19 vaccine candidate, as well as the specific potential of PE/PPE proteins as protective immunogens.
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Natural killer (NK) cell receptors (NKRs) play a crucial role in the homeostasis of antigen-experienced T cells. Indeed, prolonged antigen stimulation may induce changes in the receptor repertoire of T cells to a profile that features NKRs. Chronic antigen exposure, at the same time, has been shown to trigger the loss of costimulatory CD28 molecules with recently reported intensified antigen thresholds of antigen-experienced CD8+ T cells. In transplantation, NKRs have been shown to assist allograft rejection in a CD28-independent fashion. We discuss here a role for CD28-negative T cells that have acquired the competency of the NKR machinery, potentially promoting allorecognition either through T cell receptor (TCR) crossreactivity or independently from TCR recognition. Collectively, NKRs can bring about innate-like T cells by providing alternative costimulatory pathways that gain relevance in chronic inflammation, potentially leading to resistance to CD28-targeting immunosuppressants.
Via Krishan Maggon
Krishan Maggon 's curator insight,
August 1, 2016 3:07 AM
Trends Immunology Volume 37, Issue 8, p546–556, August 2016
Midas Seyda, Abdallah Elkhal, Markus Quante, Christine S. Falk, Stefan G. Tullius |
