Since December 2019, coronavirus disease 2019 (COVID-19) has spread rapidly around the world, causing a pandemic that threatens global public health. The causative agent of COVID-19 is Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), a novel β-coronavirus. Globally, the number of positive COVID-19 cases grows exponentially every day and now the race is on to find both an effective treatment and to develop a vaccine for prevention measures in the future.
Innate Immunity / PRR / STING
The innate immune system is crucial to limit viral infections. It relies on several groups of pattern recognition receptors (PRRs) that recognize viral nucleic acids1. These PRRs include the cytosolic DNA sensor (CDS), cyclic GMP-AMP synthase (cGAS), and the cytoplasmic RNA sensor, retinoic acid inducible gene I (RIG-I). Once activated, they induce different signaling pathways leading to the...
Autophagy is one of the three principal mechanisms used by cells to sequester, remove and recycle waste, the others being proteasomal degradation and phagocytosis. In autophagy, macromolecules in the cytosol are engulfed in a newly formed phagocytic body and subsequently digested in a special lysosome that releases the resultant metabolites back into the cytosol.
Mycoplasma contamination of cell cultures has been known for decades and disturbingly, has become widespread, threatening academic labs to biopharmaceutical production facilities. In fact, depending on the laboratory, anywhere from 10% to 85% of cell lines may be contaminated. Mycoplasmas can drastically alter your cells and consequently, skew your research results
Mycoplasma contamination of cultured cells is a massive problem in research labs and industrial facilities. In fact, depending on the setting, anywhere from 10% to 85% of cell lines might be contaminated. Mycoplasma infection can drastically alter the functions and activities of eukaryotic cells, leading to experimental artifacts and consequently, to unreliable results.
Mycoplasmas are the smallest and simplest self-replicating organisms. Due to their minimal genome, they cannot perform metabolic functions such as production of a cell wall, or synthesis of nucleotides or amino acids. Therefore, they exist strictly as parasites, using diverse organisms as hosts, including humans, animals, insects and plants.
Innate Immunity / Inflammasome
Inflammasomes are multimeric protein complexes that are crucial for host defense to infection and endogenous danger signals. They promote the secretion of the pro-inflammatory cytokines interleukin (IL)-1β and IL-18 and cause a rapid and pro-inflammatory form of cell death called pyroptosis.
Vaccine & immunoglobulin / Antibodies
Antibodies are immunoglobulin (Ig) molecules made up of 2 large heavy chains (~55 kDa each) and 2 small light chains (~25 kDa each). Heavy chains are bound to light chains by sulfhydryl linkages to form a Y shaped structure. The stem of the Y contains the constant region (Fc) and the two prongs of the Y contain the variable region (Fab). The Fab interacts with the antigen and therefore is...
Innate Immunity / STING / PRR
STING (stimulator of interferon genes), alternatively known as MPYS, TMEM173, MITA and ERIS, is a key sensor of cytosolic nucleic acids.
In the past year, an incredible amount has been revealed on the biology of STING. As the studies were published, the complexity of STING became apparent. STING, initially thought to serve solely as an adaptor protein for mediating signaling by...
Innate Immunity / PRR
β-Glucans have been consumed for many centuries for their healing properties. Since the discovery of their immunomodulating capabilities, about five decades ago, β-glucans have attracted a great deal of attention in the biomedical arena.
Innate Immunity / PRR / STING
The detection of viral and bacterial nucleic acids by the innate immune system has become an area of intense research.
Cytosolic DNA is well-known to induce the production of type I interferons (IFNs) through the STING-TBK1-IRF3 axis but the mechanism whereby it is sensed remains elusive.