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Scientists find hole in immune defenses.


Scientists find hole in immune defenses

Researchers in Switzerland report the existence of a flaw in the body's immune system immune system

Cells, cell products, organs, and structures of the body involved in the detection and destruction of foreign invaders, such as bacteria, viruses, and cancer cells. Immunity is based on the system's ability to launch a defense against such invaders.
 that allows some kinds of foreign material to evade that system, usually so efficient at seeking out, identifying and destroying invaders.

The flaw is associted with the body's self-protective mechanisms, which are built to distinguish between proteins that are naturally part of the body and the "nonself nonself /non·self/ (non´self) in immunology, pertaining to foreign antigens.

non·self
n.
That which the immune system identifies as foreign to the body.
" proteins that come from the outside. If, for example, certain nonself proteins are present on a cell, the immune-system cells know a virus has invaded that cell and it must be destroyed.

But in order not to attack its own cells, the body has to learn which proteins belong to it and which don't. If a foreign protein is similar enough to one of the body's own proteins, the invader can escape detection by the immune system, report Damir Vidovic and Polly Matzinger Polly Celine Eveline Matzinger (born 21 July 1947) is an iconoclastic scientist who proposed a novel explanation of how the immune system works, called the danger model. , of the Basel (Switzerland) Institute for Immunology immunology, branch of medicine that studies the response of organisms to foreign substances, e.g., viruses, bacteria, and bacterial toxins (see immunity). Immunologists study the tissues and organs of the immune system (bone marrow, spleen, tonsils, thymus, lymphatic , in the Nov. 17 NATURE.

Other researchers have proposed that such a flaw might exist, but Vidovic and Matzinger are the first to find a foreign protein that actually mimics a native protein, Matzinger says. Two other types of holes in the immune system have been spotted before.

One type occurs when the receptor that recognizes foreign proteins is defective. Another type is found where foreign proteins physically can't combine with native proteins that mark the body's own cells. Such a foreign protein/marker protein combination is required to alert certain immune cells.

The newly discovered flaw probably doesn't allow disease-causing organisms to slip through the body's defenses, but it may help reveal how the immune system ends up attacking the body's own cells, producing painful and debilitating de·bil·i·tat·ing
adj.
Causing a loss of strength or energy.


Debilitating
Weakening, or reducing the strength of.

Mentioned in: Stress Reduction
 autom-immune diseases such as lupus lupus (l`pəs), noninfectious chronic disease in which antibodies in an individual's immune system attack the body's own substances.  and insulin-dependent diabetes in·su·lin-de·pen·dent diabetes
n.
See diabetes mellitus.
, Matzinger says. Studies have linked such diseases to a group of immune-system genes called the major histocompatibility complex major histocompatibility complex
n.
Abbr. MHC A chromosomal segment that codes for cell-surface histocompatibility antigens and is the principal determinant of tissue type and transplant compatibility. Also called HLA complex.
, but Matzinger believes other genes must also be involved.

Such attacks on native tissue, and the lack of attacks on some foreign proteins, may be the result of the difficult compromise the body makes in trying to protect itself against invaders and accept its own tissue, Matzinger says. If the immune system learned to accept a native protein and that protein mutated, attacks on native tissue could result. If, on the other hand, the immune system tolerated differences in protein structure, it could allow organisms to invade by carrying proteins that seem to be similar to proteins found in the body.
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Author:Vaughan, Christopher
Publication:Science News
Date:Nov 19, 1988
Words:412
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