Science Featured’s Post

I'm excited to share my first scientific paper as first author. A comprehensive characterization of intestinal human intraepithelial lymphocytes in health and coeliac disease. Check out the full paper published in the European Journal of Clinical Investigation: https://lnkd.in/d5eCNK82 #immunology #celiacdisease

https://lnkd.in/gccCA4ZJ Published another groundbreaking paper in "Frontiers in Immunology". Our collaboration with Vanderbilt University, USA helped us not only diagnose this case, but publish it in a reputed journal. This paper highlights the expanding spectrum of DIAPH1 deficiency with autoimmune enteropathy being a key manifestation! #Immunology #immuneDeficiency #IBD

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

Meta-analysis and the integration of datasets can be a very powerful tool. This is an exciting article describing the auto immune disease focused meta-analysis of "public single-cell datasets of over 1.8 million peripheral CD4+ T cells from 953 individuals by projecting cells onto the reference and cataloging cell frequency and qualitative alterations of the populations in 20 diseases." Join Pythia Biosciences with 🎯 Ming "Tommy" Tang and Jenny (Ngoc) Pham for the exiting topic of single cell data integration. https://lnkd.in/gdkuVSdq #singlecell #singlecellanalysis #multiomics #immunology #autoimmunedisease #tcells #datavisualization https://lnkd.in/g59Q2KRa

HYPER-INFLAMMATION LEADS TO INNATE IMMUNE CELL EPIGENITIC REPROGRAMMING AND MEMORY PASSED ON TO PROGENY INNATE IMMUNE CELLS: COVID-19 as a paradigm system ** Hyper-inflammatory responses appear to become encoded into epigenetic memory of hematopoietic stem and progenitor cells (HSPC). ** Severe COVID-19 inflammatory memory can last for up to a year. ** In this period, this memory is passed to progeny innate immune cells, especially inflammatory, migratory, and differentiating monocyte phenotypes. ** IL-6 is an early cytokine driving this long-term epigenetic reprogramming ** Long-covid might result from this skewed differentiation program on innate immune cells. VACCINATION IS AN IMPORTANT STEP TO AUGMENT INNATE RESPONSES, TAMP DOWN VIRAL REPLICATION AND CONTROL INFLAMMATION preventing severe COVID-19. See also : "https://lnkd.in/en8jmuBt"

🚨𝐌𝐚𝐣𝐨𝐫 𝐁𝐫𝐞𝐚𝐤𝐭𝐡𝐫𝐨𝐮𝐠𝐡 𝐨𝐧 𝐈𝐁𝐃🚨 For the first time, a major trigger in inflammatory bowel disease (IBD). The breakthrough came as researchers discovered a part of DNA only active in some immune cells which causes inflammation in the bowels. Kudos to James Lee & his research team at the The Francis Crick Institute 👏🏼 As one of the 7 million people around world living with IBD, it brings me great joy seeing this. One of the hardest things to deal with is the uncertainty and how little we know about IBD!! #IBD #immunology

Function of the inflammasome👇 📎The inflammasome is a multiprotein complex that plays a crucial role in the innate immune response, particularly in the initiation and regulation of inflammation. 📎Its primary function is to detect and respond to various danger signals, such as pathogens or cellular stress, and to trigger the production of pro-inflammatory cytokines and other immune mediators. Here are some key functions of the inflammasome: 📌Pathogen Detection: The inflammasome recognizes various microbial components, including pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs). These signals can be derived from bacteria, viruses, fungi, or damaged host cells. 📌Activation of Caspases: Upon detection of danger signals, the inflammasome activates pro-inflammatory caspases, particularly caspase-1. Activation of caspase-1 leads to the processing and secretion of pro-inflammatory cytokines such as interleukin-1β (IL-1β) and interleukin-18 (IL-18). 📌Inflammatory Response: IL-1β and IL-18 are potent pro-inflammatory cytokines that play key roles in initiating and amplifying the inflammatory response. They promote the recruitment of immune cells to the site of infection or tissue damage and enhance the antimicrobial activities of phagocytes. 📌Pyroptosis: In addition to cytokine secretion, activation of the inflammasome can induce a form of programmed cell death known as pyroptosis. Pyroptosis helps to eliminate infected cells and prevent the spread of pathogens. 📌Regulation of Immune Responses: The inflammasome also modulates adaptive immune responses by shaping the activation and differentiation of T cells and influencing antibody production. 📎Overall, the inflammasome plays a critical role in host defense against infections and in the maintenance of tissue homeostasis. However, dysregulated inflammasome activation has been implicated in various inflammatory diseases, autoimmune disorders, and metabolic disorders, highlighting its importance in health and disease. Image from: Carsten Carlberg, Eunike Velleuer - Molecular Immunology_ How Science Works-Springer (2022) #inflammasome #immunesystem #immunology #cancerbiologyresearch #cancerbiology

📍 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

Immune protein linked to long COVID A signalling molecule that helps to kick-start inflammation in the lungs could play a key part in aggravating some long COVID symptoms. Previous research has shown that people with long COVID have elevated levels of the molecule, called interferon gamma (IFN-γ). By inhibiting IFN-γ in mice with COVID-19, “we were able to dampen the chronic conditions after infection”, says immunology researcher and study co-author Jie Sun. “In the future, we could target this pathway for potential treatment of long COVID.” #COVID #longCOVID #intrferongamma #IFNg #treatment https://lnkd.in/db349gPF