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The League of Extraordinary Cell Types - Immune System: T-cells 🪖 T-cells, also known as T-lymphocytes, are major contributors to the adaptive immunity in vertebrates. They send signals to the immune system to safeguard the body against threats such as viruses, bacteria, allergens and even cancerous cells. ❤️🩹 Cytotoxic T-cells and helper T-cells are the predominant types of T-cells that keep the host healthy by fighting all sorts of infections. Cytotoxic T-cells are toxic for their targets and helper T-cells help other immune cells. 🦴 T-cells originate from the bone marrow progenitor cells and migrate towards the thymus. T-cells derive their name from the thymus where they mature and differentiate into different types of T-cells. 🤢 Some common abnormalities of T-cells include DiGeorge syndrome, which prevents healthy T-cell production; Hodgkin lymphoma, cancer of the lymphatic system; AIDS/human immunodeficiency virus (HIV) which attacks the CD4+ T-cells. 💉 A major breakthrough towards the new treatment paradigm is the chimeric antigen receptor (CAR) T-cell therapy. CAR T-cell therapy is a form of immunotherapy that genetically alters a patient’s own (autologous) T-cells to fight against cancer. Stay tuned to learn more extraordinary cell types! Credit: Art by Nelli Aghekyan, Set in motion by Emanuele Petretto, PhD, Words by Suruchi Poddar, PhD, Project Coordinator: Małgorzata Maksymowicz, PhD, Series Director: Dr. Radhika Patnala #scicomm #lifescience #Extraordinarycelltypes About the series: The League of Extraordinary Cell Types The team at Sci-Illustrate and Endosymbiont bring to you an exciting series where we dive deep into the wondrous cell types that make our bodies tick ❤. ____________________________________________ Tag someone you know working in this field and help us find them 😊 If you enjoyed this content, make sure to follow us not to miss a post!

Learn more about the terminators of our immune system in this article. https://lnkd.in/efVeXHu4

People with long COVID have dysfunctional immune cells that show signs of chronic inflammation and faulty movement into organs, among other unusual activity, according to a new study by scientists at Gladstone Institutes and UC San Francisco (UCSF). The team analyzed immune cells and hundreds of different immune molecules in the blood of 43 people with and without long COVID. They delved particularly deep into the characteristics of each person’s T cells—immune cells that help fight viral infections but can also trigger chronic inflammatory diseases. Their findings, which appear in Nature Immunology, support the hypothesis that long COVID may involve a low-level viral persistence. The study also reveals a mismatch between the activity of T cells and other components of the immune system in people with long COVID. “Our results are an essential first step to understanding what’s going on with T cells in long COVID,” says senior author Nadia Roan, PhD, a senior investigator at Gladstone and a professor at UCSF. “This paves a path toward answering ongoing questions about the different types of long COVID, the mechanisms that cause it, and how to treat and prevent it.” Read more: https://bit.ly/3SfbGQX

A new platform for therapies against cancer and more The COVID mRNA vaccine works by inducing the body to produce its own safe version of the SARS-CoV-2 spike protein and train the immune system to recognize and disable it, then do the same once it encounters the actual virus. This approach — used successfully for the first time against SARS-CoV-2 — has become the blueprint for harnessing the body’s immune responses to produce its own “therapy” against various infectious diseases as well as multiple types of cancer, several forms of heart disease, rare diseases such as cystic fibrosis, and certain autoimmune conditions. https://lnkd.in/giXCdNsn

📍 Acquired Immune Deficiency Syndrome correlation with SARS-CoV-2 N genotypes Excerpt: Background Epigenetics and clinical observations referring to Betacoronavirus lead to the conjecture that Sarvecovirus may have the ability to infect lymphocytes using a different way than the spike protein. In addition to inducing the death of lymphocytes, thus drastically reducing their population and causing a serious immune deficiency, allows it to remain hidden for long periods of latency using them as a viral reservoir in what is named Long-Covid Disease. Exploring possibilities, the hypothesis is focused on that N protein may be the key of infecting lymphocytes. Method The present article exhibits a computational assay for the latest complete sequences reported to GISAID, correlating N genotypes with an enhancement in the affinity of the complex that causes immune deficiency in order to determine a good docking with the N protein and some receptors in lymphocytes. Results A novel high-interaction coupling of N-RBD and CD147 is presented as the main way of infecting lymphocytes, allowing to define those genotypes involved in their affinity enhancement. Conclusion According to the results of the In-Silico, it is evidenced a natural evolution of the Betacoronavirus genera in order to balance propagation, infectivity and persistence. The main genotypes are evidenced in S/493, S/484, N/120 and N/152. Optimizing S/493 and S/484 means better airborne spread by infecting more the lungs and nasopharyngeal tissue meanwhile N/120 and N/152 genotypes reduce the Immune Response infecting lymphocytes allowing the virus to persist indefinitely, causing an Acquire Immune Deficiency Syndrome and other related syndromes to chronic viremia, especially with viruses that cause respiratory and blood diseases. ➡ https://lnkd.in/dHQ4gS-8 #longcovid #lymphocytes #AcquiredImmuneDeficiency #artificialintelligence #immuneevasion #Betacoronavirusgenera

Extremely excited to see our paper is out in #Nature! How does the body respond to SARS-CoV-2, and what happens if you don't get infected after exposure? We unraveled the exact timeline of the cellular responses to inoculation with SARS-CoV-2 in humans. By applying single cell multiomics to a unique SARS-CoV-2 human challenge model, we uncovered the identity and timeline of the local and systemic immune responses to viral exposure. We used this approach to uncover a multitude of both fundamental and translational insights into how our immune system functions to protect us against viral infections when there is no immunological memory available yet. In addition, while none of the inoculated individuals had pre-existing immunological memory, more than half of them did not develop a sustained infection, which gave us the unique opportunity to also study the immune responses that prevented infection after viral exposure. Highlights of our work include dozens of novel time-restricted response states, including unexpected timing of interferon signalling, new innate responses in unexpected cells and in non-infected cases, identification and application of new activated T cell populations, and lower HLA-DQA2 expression as predictor for sustained infections. But there're many more cool findings that can be found in our manuscript! This has been an amazing team effort by the the labs of Sarah Teichmann FMedSci FRS and Marko Nikolić. Special thanks to my partners in crime Kaylee Worlock and Lisa Dratva, and the Chiu lab that established the model. With awesome teams from Wellcome Sanger Institute, UCL, The Netherlands Cancer Institute, Imperial College London, and hVIVO. Big thanks to everyone involved!

🚨 New Special Issue Alert! 🚨 🌐 Evasion of Host Immune System in Viral Oncogenesis 🌐 Virus-induced cancers, driven by viruses like Epstein-Barr (EBV), Kaposi’s Sarcoma Herpesvirus (KSHV), Human T-cell Leukemia Virus-1 (HTLV1), human papillomavirus (HPV), and hepatitis B & C (HBV, HCV), present a serious global health challenge. These viruses employ various strategies to evade the host immune system, creating a favorable environment for cancer development. Key mechanisms include: 🔸 Downregulation of MHC molecules 🔸 Disruption of innate immune signaling 🔸 Manipulation of immune checkpoint pathways 🔸 Orchestration of oxidative stress Understanding these strategies is critical to developing targeted immunotherapies and vaccines to fight virus-associated cancers. 📅 Submission Deadline: 31 May 2025 📍 Guest Editor: Prof. Shunbin Ning, Quillen College of Medicine, East Tennessee State University, USA 🔗 Learn more and make new submissions: https://lnkd.in/eWQ_uY4g #EBV #HTLV1 #KSHV #ImmuneEvasion #ViralOncogenesis #CancerResearch #Immunotherapy #MedicalResearch #OncologyResearch #TechSciencePress

#genetherapy #oncolyticvirus #glioma #virotgerapy #adenovirus #oncolyticvirus Overcoming Immune Barriers in Glioma Therapy with a Novel Chimeric Oncolytic Adenovirus Neutralizing antibodies limit the efficacy of oncolytic virus treatments in glioma patients, but a chimeric virus, Delta-24-RGD-H43m, shows promise by evading these antibodies and improving long-term survival, offering a new treatment strategy for patients with immunity against previous oncolytic adenovirus therapies. https://lnkd.in/gZxFz79C

MIRROR REFLECTION: The Power of Restoring Th1/Th2 Balance AlloStim® is a groundbreaking immunotherapy designed to empower your immune system to do what it does best—protect against cancers and infectious diseases. The immune system has two polarized components, normally maintained in a carefully regulated balance. On one pole are Th1 cells which mediate cellular immunity and help to protect against cancers and viruses; and, on the other pole are Th2 cells which mediate humoral (antibody) immunity and help to neutralize parasites and pathogens that reside outside of cells. A shift of Th1/Th2 cell subsets toward Th2 dominance occurs in malignant tumors. The same type of shift towards Th2 biased responses occurs in the elderly, making the elderly more susceptible to cancer and viral diseases. Many cancers and viruses actually promote a "Th2-dominant" environment in order to avoid immune elimination. AlloStim® is designed to correct Th1/Th2 imbalances by increasing Th1 cell titers in circulation, which works to restore cell mediated immunity in both cancer patients and the elderly. AlloStim® thus changes the game, by broadly restoring immune surveillance and promoting cellular immune attacks on cancer and viral infected cells. Both cancer patients and the elderly have an imbalance in Th1/Th2 ratios with a loss of Th1 cellular immune function. The ability of AlloStim® to correct Th1/Th2 imbalance by increasing Th1 cell titers is the reason the same experimental drug is in clinical development both in late stage metastatic cancer patients and healthy elderly adults. We’re excited to be pushing the boundaries of what immunotherapy can do to restore the power of the immune system to protect against and eliminate disease. #immunotherapy

Thank you @Frontiers in Immunology for providing this opportuniety to serve as an Editor for the articles on "CEACAM". This has definitely added to the pool of our knowledge on usefulness of this molecule and its application in immune modulation. This special issue is dedicated in the memory of my mentor, collaborator, amazing scientist, and a wonderful friend Bernhard Singer who inspired many in the CEACAM field. #immunology #cancerresearch #pathogens