German researchers have discovered why nickel causes allergies so often: Individual particles released from the metal attach to a key protein in the immune system, which is usually responsible for detecting invading bacteria. This triggers an inflammatory reaction that eventually leads to the typical symptoms of contact allergy, such as redness, burning, itching and sometimes even blistering. Interestingly, the docking site for the nickel particles does not match that for the bacteria. If it were thus possible to block the nickel site in a targeted manner, it would be possible to deal effectively with the nickel allergy without at the same time disturbing the function of the protein, which is important for the immune system. Up to ten percent of all women and one percent of men in industrialized countries suffer from a nickel allergy. It arises when the skin comes into contact with the metal and becomes sensitized. After that, even a brief touch with nickel-containing objects can trigger violent eczema. Although medical experts have long known that this allergy belongs to the so-called late-type allergies. Antibodies do not trigger the symptoms, as with many other allergies, but T cells, a form of white blood cells. In addition, it was already known that sensitization only takes place if, in addition to T-cell mobilization, there is another signal that promotes inflammation. Its identity was previously unknown.
It seems to be a receptor called TLR4, which is located on the surface of certain immune cells, Schmidt and his colleagues could now show with the help of genetically engineered mice. It is a protein molecule in whose castle-like recognition site the molecule LPS, a component of the outer envelopes of bacteria, fits exactly. Also, nickel ions that dissolve out of the moisture of the skin from nickel-containing materials can dock to the receptor? Although in a different place, but with the same consequences: They trigger as well as the bacteria from a series of reactions that ultimately lead to violent inflammation at the contact point.
TLR4 is an old acquaintance of allergy researchers: Among other things, it is responsible for allergic reactions to the excrement of house dust mite. The mechanism works differently. However, the reaction to nickel has a decisive advantage, the scientists write: It can be blocked without affecting the sensitivity of the receptor for LPS and thus for invading bacteria. And another interesting finding the researchers owe the study: Only the human TLR4 receptor reacts in this way to the metal ions? the mouse variant is immune to nickel. Consequently, the common practice of investigating the allergy potential of chemical substances in animal models is to be treated with great caution, write Schmidt and his team.
Marc Schmidt (University of Heidelberg) et al .: Nature Immunology, online pre-publication, doi: 10.1038 / ni.1919 ddp / science.de? Ilka Lehnen-Beyel advertisement