Uncovering how a special class of lethal T-cells can get out of control during the onset of inflammatory bowel disease?

!-- 22, 2020 / -- Approximately 6-8 million people worldwide suffer from inflammatory bowel disease, a chronic intestinal disease that induces the appearance of the abdomen. Pain, urgent frequent detocation, blood stools and weight loss; a new study suggests that a failure of a member of the patient's own immune system called killer T-cells may be one of the culprits for inflammatory bowel disease, a finding that could provide new clues for scientists to develop new treatments for inflammatory bowel disease.
Photo Source: John Chang's inflammatory bowel disease is divided into two types, ulcerative colitis, which affects colon tissue, and Crohn's disease, which affects the entire digestive tract; researchers believe that when the body's overactive immune system attacks harmless bacteria in the gut, inflammatory bowel disease is induced, and although there are many treatments for inflammatory bowel disease, there is no effective long-term treatment, which leaves many patients with no better treatment options.
In one study, researchers analyzed immune cells from the blood and intestines of healthy individuals and compared them with cells in the body of patients with ulcerative colitis, revealing the molecular mechanisms of immune system dysfunction in patients with inflammatory bowel disease; There are many reasons for this, but one reason scientists don't fully understand how the immune system is involved in inflammatory bowel disease, and they hope that in-depth research will fill the gap in the study and develop a new strategy for treating inflammatory enteropathy by targeting the right immune cells.
The immune system is divided into congenital immune systems, the former being the body's first line of defense, which can act quickly in minutes to hours, but the system generally only perceives changes caused by microorganisms and does not respond specifically to specific pathogens, meaning that some intruders are ignored.
the adaptive immune system can detect special threats, but its response speed is slow, often takes a few days to start, T cells are part of the adaptive immune system, which can be further divided into CD4 plus and CD8 plus T cells.
CD4 plus T cells are helpers to help other immune cells, which can induce inflammation by releasing soluble molecules called cytokines, while CD8 plus T cells can also release cytokines, but their primary function is to kill cells infected by microbial invaders, which is why CD8 plus T cells are often referred to as "serial killers".
When the infection is cleared, the pathogens are eliminated, and cells called memory T cells will continue to exist, allowing them to remember the pathogens they encountered, and if they encounter the pathogen again, they will initiate a stronger and faster response than the first time, while these memory T cells and their descendants will survive longer in the body, even decades in the event of infection with pathogens such as measles. the
vaccine was developed to provide the body with a set of microbial pathogens to be previewed so that the host immune system can build an army of memory cells to help fight infectious pathogens such as SARS-CoV-2, so that if the virus attacks again, memory T cells will act quickly to activate the host immune system, including promoting B cells to produce antibodies.
Memory T-cell researchers who resided in tissues divided memory T-cells into sub-groups based on whether and where they wandered in the body, where circulating memory T-cells were scouts who could look for signs of infection by patrolling the blood, lymph nodes and spleen; Memory cells (TRMs) are sentinel stationed at key entrances to the body, including the skin, lungs and intestines, which act quickly to respond to infectious threats, while TRM in the intestines also has a peacekeeping force-like function and does not tend to overreact to the many harmless microorganisms that live in the intestines.
researchers analyzed blood and intestinal samples from participants and found that there were at least four different varieties of CD8 plus TRM in the gut, each with a unique function.
Photo Source: University of Cambridge researchers have found that individuals with ulcerative colitis have higher numbers and proportions of TRM belonging to the four different varieties mentioned above, a cell type they call inflammatory TRM, which produces large amounts of cytokines and protein factors and helps kill other types of cells, and that high levels of specific cytokines induce inflammation and tissue damage in the body.
In patients with ulcerative colitis, the balance of memory cells is transferred to this inflammatory TRM group, which becomes part of the problem by promoting persistent inflammation and tissue damage.
In addition, the researchers found that these inflammatory TRMs may still be present in the intestinal tissue and enter the bloodstream, while other studies in mice and human bodies have shown that TRM can still leave the tissue in some cases despite the presence of tissue; Inflammatory TRM may wander away and cause damage in other parts of the body, which may help explain why autoimmune diseases (such as inflammatory bowel disease in the digestive tract or psoriasis on the skin) from one organ of the body can affect other parts of the body.
Inflammatory bowel disease and other autoimmune diseases may be characteristic of memory-related memory T-cells, making it ideal for developing vaccines that can survive longer in the body and produce a stronger immune response when the same microbe invades for the second time, which may explain why autoimmune diseases tend to be chronic and lifelong.
It should be noted that none of the current drugs for inflammatory bowel disease have been developed specifically for long-lived memory cells, which may be one reason why these therapies do not work in many patients' bodies, and the researchers suggest a therapy that targets and destroys inflammatory TRM, but may induce side effects such as suppressing the host immune system and increasing the risk of infection in patients.
The findings are based on previous studies that have found that different TRM subsystypes, such as CD4-T cell subtypes, may also be involved in the development of inflammatory bowel disease, while other studies have found that TRM plays a critical role in the development of autoimmune diseases that affect other organs, such as the skin and kidneys.
the possibility of memory T cells co-existing in inflammatory bowel disease is incredible to researchers, but they don't know much about TRM, can they selectively target inflammatory TRM destruction? Is there a cure for inflammatory bowel disease? Wait, it may take further research by later scientists to answer, and researchers will delve into the link between TRM and inflammatory bowel disease.
() !-- /ewebeditor: page -- !--ewebeditor: page title"--reference: 1 The global, regional, and national burden of education bowel disease in 195 countries and territories, 1990-2017: a system analysiss for the Global Burden of Disease Study 2017 (2) Crohn's disease (3) Ulcerative colitis (4) Voicey Diseases (5) Interconnected subsesses to memory fic. Helper T cells have different effector functions (6) Heterogeneity and clonal relationships of adaptive immune cells in ulcerative colitis revealed by single-cell analyses (7) Agenting and Tissue-Resident CD4 and T Cells With Reactivity to Intestinal Microbio Areta Areta Healthy Personal and Functional AlterIs Rogue iningy bowel disease !-- / ewebeditor: page--