Lymphocytic choriomeningitis, or LCM, is a rodent-borne viral infectious disease that presents as aseptic meningitis (inflammation of the membrane, or meninges, that surrounds the brain and spinal cord), encephalitis (inflammation of the brain), or meningoencephalitis (inflammation of both the brain and meninges). Its causative agent is the lymphocytic choriomeningitis virus (LCMV), a member of the family Arenaviridae that was initially isolated in 1933. Although LCMV is most commonly recognized as causing neurological disease, as its name implies, infection without symptoms or mild febrile illnesses are common clinical manifestations. Additionally, pregnancy-related infection has been associated with congenital hydrocephalus, chorioretinitis, and mental retardation.
NIH investigators and colleagues have discovered that when the immune system first responds to infectious agents such as viruses or bacteria, a natural brake on the response prevents overactivation.
A UCLA research team has identified a new paradigm for understanding the regulation of the immune system, potentially paving the way for new approaches to treating infections and immune-related diseases such as type 1 diabetes and certain cancers.
A new study published in the journal Cell Reports reports a novel method by which antitumor drugs that focus on reawakening exhausted immune cells called cytotoxic T cells against cancer can be quickly identified. This could help treat a large subset of cancers that thrive because of their ability to suppress antitumor activity in T cells.
Scientists at Scripps Research have developed a method for rapidly discovering potential cancer-treating compounds that work by resurrecting anti-tumor activity in immune cells called T cells.
Researchers at the CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences identified a key mechanism for how antiviral immune responses reprogram liver metabolism. Their recent study, which was published in the renowned scientific journal Immunity, investigated the communication between inflammation and liver metabolism during chronic viral infection.
Many of the world's most common or deadly human pathogens are RNA-based viruses -- Ebola, Zika and flu, for example -- and most have no FDA-approved treatments.
Memory T cells are a critical element of our immune system's historical archive. To prevent repeat infections, these cells retain a record of germs they've fought before.
Swiss scientists from the University of Geneva, Switzerland, and the University of Basel have created artificial viruses that can be used to target cancer.
Immune diseases like multiple sclerosis and hemophagocytic lymphohistiocytosis unleash destructive waves of inflammation on the body, causing death or a lifetime of illness and physical impairment.
Life is a question of balance, and the body is no exception. Expression levels of certain proteins can affect the immune system's ability to neutralize a virus.
Scientists at the Gladstone Institutes discovered that the vaginal immune system is suppressed in response to RNA viruses, such as Zika.
In a new study with broad implications for treating cancers and chronic viral infections, scientists at The Scripps Research Institute (TSRI) have uncovered a mechanism behind a phenomenon called “T cell exhaustion.”
Reprogramming of the molecular pathways underlying normal metabolism is essential for T cell infection-fighting function and for the immune system to form a "memory" of the microbes it has already encountered. But exactly how metabolism in exhausted T cells is maintained in chronic infections and cancer is a missing element in this line of research.
Research led by scientists at the Sanford Burnham Prebys Medical Discovery Institute has identified a new regulator of immune responses. The study, published recently in Immunity, sheds new light on why T cells fail to clear chronic infections and eliminate tumors.
For the first time, scientists at The Scripps Research Institute (TSRI) have solved the structure of the biological machinery used by a common virus to recognize and attack human host cells.
Sometimes even cells get tired. When the T cells of your immune system are forced to deal over time with cancer or a chronic infection such as HIV or hepatitis C, they can develop 'T cell exhaustion,' becoming less effective and losing their ability to attack and destroy the invaders of the body.
Hemorrhagic fevers caused by Lassa, dengue and other viruses affect more than one million people annually and are often fatal, yet scientists have never understood why only some virus-infected people come down with the disease and others do not.
Scientists at Emory Vaccine Center have shown that an immune regulatory molecule called IL-21 is needed for long-lasting antibody responses in mice against viral infections.
St. Jude Children's Research Hospital study shows how compounds blocking an enzyme universal to all influenza viruses may allow development of new antiviral drugs that also avoid the problem of drug resistance
Scientists from The Scripps Research Institute have shown a single protein can make the difference between an infection clearing out of the body or persisting for life. The results also show where the defects occur in the immune system without the protein and offer the possibility that targeting this signaling pathway could be beneficial for treatment of persistent viral infections in humans.