immune response

04/24/2014 - 07:33

Pseudomonas aeruginosa is a bacteria that commonly infects the lungs of cystic fibrosis patients, often with lethal consequences. A cationic antimicrobial peptide called LL-37 produced from neutrophils, one of the major cellular components of the innate immune response, can induce mutations in P. aeruginosa bacterial DNA that can paradoxically increase bacterial lethality. This is the major finding of a new study in the journal PLoS Pathogens from a team of researchers in different US institutions.

 

04/14/2014 - 10:07

The immune response is delicately balanced to ensure that non-self ‘invaders’ are expelled while self-elements are tolerated. Multiple processes and mediators cooperate to maintain this balance, including the process of apoptosis, or programmed cell death. A new study published in the journal Cell Death and Disease suggests that key inhibitors of apoptosis are central to maintaining this delicate balance.

 

03/04/2014 - 10:41

Scientists in Freiburg may have discovered a fundamental aggravating factor in autoimmune diseases. If B-lymphocytes lack the protein PTP1B, the cells will become hyperactive for stimulatory signals and can thus promote an autoimmune attack. This study offers an additional explanation to how B-cells regulate an immune response.

 

02/10/2014 - 13:39

A team led by scientists at The Scripps Research Institute (TSRI) has discovered an unusual bacterial protein that attaches to virtually any antibody and prevents it from binding to its target. Protein M, as it is called, probably helps some bacteria evade the immune response and establish long-term infections.

 

02/04/2014 - 12:05

Lyme disease is often evident by a rash on the skin, but infections do not always produce similar rashes. This can make it difficult to detect the disease early, when antibiotic treatment is most effective. In the February 4th issue of the Biophysical Journal, published by Cell Press, researchers describe a new mathematical model that captures the interactions between disease-causing bacteria and the host immune response that affect the appearance of a rash and the spread of infection.