innate immune system tagged posts

The fruit fly intestine shares much of the same physiology of the human intestine, just simpler and on a smaller scale. Credit: Adam Wong, PhD. Modified from Disease Models & Mechanisms. doi: 10.1242/dmm.023408.

Study teases out how ‘good bacteria’ keep us metabolically fit. The innate immune system, our first line of defense against bacterial infection, has a side job that’s equally important: fine-tuning our metabolism. The study, led by Paula Watnick, MD, PhD, of the Division of Infectious Diseases at Boston Children’s Hospital, reveals that innate immune pathways, best known as our first line of defense against bacterial infection, have a side job that’s equally important.

In the intestine, digestive cells use an innate immune pathway to respond to harmful bacteria...

An intrinsic complement-NLRP3 axis regulates human TH1 responses. T cell receptor activation and CD46 costimulation trigger NLRP3 expression and intracellular C5a generation. Subsequent intracellular C5aR1 engagement induces ROS production (and possibly IL1B gene transcription) and NLRP3 assembly, which in turn mediates IL-1β maturation. Autocrine IL-1β promotes TH1 induction (IFN-γ production) but restricts TH1 contraction (IL-10 coexpression). C5aR2 cell surface activation by secreted C5a negatively controls these events via undefined mechanisms. Dysfunction of this system contributes to impaired TH1 responses in infection or increased TH17 responses during intestinal inflammation.

Researchers have unlocked secrets of our ancient immune system...

beta-amyloid fibrils propagate from yeast surfaces and capture Candida albicans in culture medium. Credit: D.K.V. Kumar et al. / Science Translational Medicine (2016)

A new study from Massachusetts General Hospital (MGH) investigators provides additional evidence that amyloid-beta protein, deposited in the form of beta-amyloid plaques in Alzheimer’s disease – is a normal part of the innate immune system, the body’s first-line defense against infection. Expression of human amyloid-beta (A-beta) was protective against potentially lethal infections in mice, in roundworms and in cultured human brain cells. The findings may lead to potential new therapeutic strategies and suggest limitations to therapies designed to eliminate amyloid plaques from patient’s brains.

“Neurodegeneration in Alzheime...

Highlights •MYSM1 inhibits PRR pathways for pro-inflammatory and type I IFN gene induction •MYSM1 transiently accumulates in the cytoplasm upon microbial challenge •MYSM1 interacts with and inactivates TRAF3 and TRAF6 via its SWIRM and MPN domains •MYSM1 protects against sepsis but renders mice more susceptible to viral infection

Our immune system is vital to us and can sometimes overreact causing chronic illnesses, such as for instance rheumatism and allergy. Now, researchers have identified a molecular switch – MYSM1 – that can suppress such an overreaction and avoid inflammation.

“The discovery of MYSM1 is a major milestone in our understanding of how our immune system works, and how its response could be controlled in order to prevent inflammatory diseases such as sepsis,” ...