![]() |
|
Saturday, February 4th 2012 |
|
Infectious Disease
Infectious diseases pose one of the world's leading healthcare problems. Especially in developing countries, infectious diseases cause the premature death of millions and millions of people each year, leading to enormous suffering and a serious disruption of social and economic development. Vaccination programs have been successful in the Western world (e.g. polio, smallpox, measles), but in poor countries, the lack of organized healthcare systems and sufficient funds allows these diseases still to make numerous victims. Furthermore, for many of today's main infectious diseases, such as Tuberculosis, HIV/AIDS, and malaria, vaccines are not available.
Problem
It is still not clear why an infectious agent (virus, parasite, bacterium) causes disease in one individual, but not in another. Insight into the genetic mechanisms that form the basis of an individual's response to infection is needed to understand what the mode of action of vaccines should be. Only then can we develop efficient vaccines for different people.
There is already a lot of knowledge on pathogen-host interactions, disease pathogenesis, immune responses etc., but it is fragmented. To create an overall picture of the complex network of interactions involved in infectious disease, we need to combine the current knowledge and fill in the gaps. Approach
The focus of CMSB is on the cascade of reactions initiated by the so-called dendritic cells. Dendritic cells (DC) act as sentinels; they continuously sample their immediate environment for any foreign substances. Their mode of action is extremely fast, upon sampling they need to decide immediately whether the substance is self or non-self. DCs interact with helper cells (CD40), who in turn can activate T-cells (killer cells). It is obvious that disruption of this system can have serious consequences; either a pathogen is not recognized and can enter the body or the body's own tissue is seen as threatening, causing auto-immune responses.
The genetic basis and regulation of the DC system is extremely important. Malfunctioning of this system is not only associated with infectious disease, but also with for example Alzheimer's disease. Here, the amyloid plaques formed in the brain are apparently not recognized by the body and therefore not degraded and cleared away. It is thought that inflammation processes in the blood vessels play a role in the disruption of the system. This is also likely to be the case in atherosclerosis. Furthermore, auto-immune diseases are also connected to disruptions of the immune system. Tuberculosis (TB) will act as the case-study. Basic knowledge generated from studying TB will also contribute to our understanding of the complex cellular processes involved in other conditions, such as Hepatitis C, leprosy, malaria and Human Papilloma Virus related infections. Objectives
To make substantial progress in our basic and detailed understanding of the body's response to infections and the role and regulation of the dendritic cell systems in this overall process. And to use that knowledge to develop new preventive and therapeutic vaccines. In addition, our findings may contribute to new biological therapies for auto-immune diseases and inflammatory conditions.
|
|
|||||||||
|
© 2003 - 2012 CMSB |
|||||||||||