Podcasts about cytotoxic t

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.23.218529v1?rss=1 Authors: Banerjee, S., Majumder, K., Gutierrez, G. J., Gupta, D., Mittal, B. Abstract: The novel Corona Virus Disease (COVID-19) pandemic has spread a blaze of increasing fatality rates across the world. The dearth of potential vaccines has left the survival of mankind with doubts. The development of multi-epitope vaccine in this current situation could be a possible COVID treatment. We have designed a novel multi-epitope, multi-protein vaccine with different proteins of Severe Acute Respiratory Syndrome - Corona Virus -2 (SARS-CoV-2) with immuno-informatics approaches, which has been validated in silico to be stable and potential. It has been prepared with Cytotoxic T-cell (TC ) and Helper T-cell (TH ) cell binding epitopes overlapping with B-cell binding epitopes predicted for 6 proteins conserved among 4 different viral strains isolated across the world. Both the humoral and cell-mediated immune responses are ensured due to the presence of T cell and B-cell inducing epitopes along with interferon-gamma inducing epitopes. The final vaccine construct comprises of an adjuvant at the N terminal, Cytotoxic T Lymphocyte and Helper T Lymphocyte epitopes. The construct showed potential antigenicity and was non-allergic. The molecular docking of the refined, validated tertiary structure model of the vaccine was performed with immune-stimulatory Toll Like Receptors (TLR), TLR-2,3,4. The molecular dynamics simulations of docking revealed binding interactions of receptor with vaccine. The immune simulation of the vaccine even confirmed the initiation of elevated host immune responses. The efficient translation of the vaccine in an expression vector was confirmed with in-silico cloning approach. Certainly, the development of such vaccine candidate could possibly be an effective therapy for COVID-19. Copy rights belong to original authors. Visit the link for more info

Cytotoxic T cells use Flower power In order to efficiently kill multiple target cells, cytotoxic T lymphocytes must endocytose and recycle cytotoxic granule membrane components from the immunological synapse. Chang et al. reveal that a protein called Flower facilitates granule endocytosis in a calcium-dependent manner. This biosights episode presents the paper by Chang et al. from the February 5th, 2018, issue of the Journal of Cell Biology and includes an interview with one of the paper's senior authors, Jens Rettig (Saarland University, Saarbrücken, Germany). Produced by Caitlin Sedwick and Ben Short. See the associated paper in JCB for details on the funding provided to support this original research. Subscribe to biosights via iTunes or RSS View biosights archive The Rockefeller University Press biosights@rockefeller.edu

In this video we see a killer T cell of the immune system attacking a cancer cell. Professor Gillian Griffiths: “Cells of the immune system protect the body against pathogens. If cells in our bodies are infected by viruses, or become cancerous, then killer cells of the immune system identify and destroy the affected cells. Cytotoxic T cells are very precise and efficient killers. They are able to destroy infected or cancerous cells, without destroying healthy cells surrounding them. The Wellcome Trust funded laboratory of Professor Gillian Griffiths, at the Cambridge Institute for Medical Research, investigates just how this is accomplished. By understanding how this works, we can develop ways to control killer cells. This will allow us to find ways to improve cancer therapies, and ameliorate autoimmune diseases caused when killer cells run amok and attack healthy cells in our bodies.” Cytotoxic T cells are just 10 microns in length: approximately one-tenth the width of a human hair. These movies are 92 times real time. The original footage shown was made by Alex Ritter, a PhD student on the NIH-OxCam programme, in the laboratory of Professor Gillian Griffiths at the Cambridge Institute for Medical Research and the Department of Medicine of the Clinical School of the University of Cambridge. The images were acquired using an Andor Revolution spinning disk system with an Olympus microscope. Professor Griffiths is a Wellcome Trust Principal Research Fellow. Links for more information: http://www.cimr.cam.ac.uk http://www.immunology.cam.ac.uk/about Music by Intercontinental Music Lab http://www.intercontinentalmusiclab.com

The study is subdivided into two different parts: the first part deals with the development of a method to gain uterus milk in vivo during the preimplantation periode in cattle for the investigation of regulatory factors. The second part investigates different proteases in bovine follicles 20 hours after GnRH (Gonadotropin releasing hormone) injection (shortly bevor ovulation) for comparable as well as in the corpus luteum (CL) during oestrous cycle and induced luteolysis. In addition apoptotic as well as anti-apoptotic factors were evaluated in the CL during oestrous cycle and induced luteolysis. For the development of a method for gaining uterus milk in vivo during the first 24 days of gravidity in cattle, nine heifers were cycle synchronised using the Ovsynch method and artificially inseminated. Before flushing an epiduralanaesthesia was given and both uterus horns were flushed with 13ml 0.9% NaCl using a balloon embryo transfer catheter at day 5, 7, 12, 17 and 24 of gravidity. The catheter was placed 1cm cranial to the bifurcatio uteri in both horns. It was possible to retrive between 3ml and 13ml of the used flushing fluid. The uterus milk from the ipsilateral horn was inspected for an embryo and an EDTA-stabilisator was given to the uterus milk of both horns. An infection of the uterus occured in three heifers after the second and in five heifers after the third flushing. In one heifer no infection was found. Between day 17 and day 24 all heifers showed clear signs of oestrus. It was possible to detect progesterone, oestradiol-17-beta, PGF2alpha and VEGF via enzyme immunoassay (EIA) and radio immunoassay (RIA), respectively. Because of the occurred infection no statistic analysis was made. But it could be seen that the level of progesterone ranged between

Cytotoxic T cell responses to the murine Cytomegalovirus (MCMV) were elicited in BALB/c mice (H-2d) by infectious virus. Eight days after infection, MCMV-primed local lymph node T cells were either depleted for T cells expressing a V beta 8+ TCR or separated into V beta 8+ and V beta 8- subpopulations by a cell sorter using the mAb F23.1. T cells were then expanded in vitro under limiting dilution conditions in the presence of IL-2 and in the absence of viral Ag to avoid selection by Ag in vitro. Frequencies of CTL precursors specific for the Immediate- Early-Ag 1 of MCMV and restricted to H-2Ld were determined. L cells of the endogenous haplotype H-2k cotransfected with the genes for MCMV-IE 1 and H-2Ld were used as target cells. Detection of a CTL response required previous priming of the animals by infection in vivo (less than 1/10(6) for nonimmunized animals). In primed animals CTL precursors of this specificity and restriction were three to fivefold more frequent in the V beta 8+ population (1/9.900 to 1/22.300) than in the V beta 8- population (1/57.000 to 1/87.200). Control experiments showed that frequencies were not influenced by the treatment with the anti-V beta 8-antibody and the fluorescein-labeled anti-Ig itself. V beta 8+ and V beta 8- T cells did not reveal any frequency differences when several other responses were determined (TNP-specific self- restricted CTL precursor; Th cells specific for keyhole limpet hemocyanin or Listeria monocytogenes).

CYTOTOXIC T cells lyse only those virus infected target cells in vitro which express, in addition to the viral antigen(s), those K or D region products of the major histocompati-bility complex (MHC) which were present during anti-viral sensitisation in vivo. This 'associative recogniton' by cytotoxic T cells could reflect the interaction of two T-cell receptors with specificity for target K or D gene products and independently for the viral antigen, or one receptor with specificity for virally altered K or D region products (see ref. 1 and refs therein). There are various ways that the MHC antigens could be altered, including 'modification from within', where the virus modifies host protein synthesis by interfering with transcription2, translation or post-translational glycosylation; or 'modification from without' where enzymic or chemical alteration of cell membrane proteins are induced by virus activity at the cell surface. In this report we show that inactivated Sendai virus or isolated Sendai virus envelopes can serve to modify a cell and make it a specific target for Sendai-immune T-cell killing, thus excluding the possibility of 'modification from within' in this system.