Tuberculosis Bacteria May Protect Against Autoimmune Disease


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Dr. Kerlero de Rosbo and Prof. Ben-Nun. Selective enhancement

Institute researchers have identified a bacteria-derived protein that protects animals from experimental autoimmune encephalitis (EAE), a disease closely resembling multiple sclerosis (MS) in humans.

This research provides a potential starting point for designing additional drugs for multiple sclerosis, a disease in which the destruction of myelin leads to muscle weakness and paralysis. Two medications for multiple sclerosis -- copolymer-1 and interferon-beta -- have already emerged from other Weizmann Institute laboratories.

This latest finding is an outgrowth of Institute studies into the unexpected effects of specific bacteria on experimental autoimmune diseases. Participating in this work, described in the Journal of Immunology, were Prof. Avraham Ben-Nun of the Department of Immunology, Australian visiting scientist Dr. Nicole Kerlero de Rosbo and graduate students Itzhak Mendel and Gregor Sappler.

It has long been know that when tuberculosis bacteria are injected into mice together with myelin basic protein -- a component of nerve tissue and a weak stimulator of an animal's immune system -- the bacteria cause the immune system to "overwork," and the mice develop full-blown nerve-damaging EAE. However, a 1992 study by Prof. Ben-Nun and departmental colleague Dr. Dan Lehman showed that under certain circumstances the very same bacteria produce the reverse effect and protect the mice from EAE. In the latest study, Ben-Nun and his team identified a specific bacterial protein that provides this protective activity.

In both EAE and multiple sclerosis, the body's immune system attacks scattered areas of the brain and spinal cord, causing inflammation and also stripping nerve fibers of their insulating myelin sheaths, thus impairing their ability to conduct impulses. The Institute team found that the newly-discovered bacterial protein can provide effective protection because it selectively enhances the production of immune-system T cells without stimulating the production of the T cells that attack myelin.

Prof. Ben-Nun holds the Eugene and Marcia Applebaum Chair