A research team by Chang Gung University and Chang Gung Memorial Hospital yesterday said it is the first to discover the pathogenesis of a rare disease — the anti-interferon-gamma autoantibodies disease.
Anti-interferon-gamma autoantibodies disease is a rare disease discovered in 2005, and starting from 2012, more people with the disease were found in Thailand and Southeast Asian countries, for a total of more than 200 cases — with more than 70 cases confirmed in Taiwan.
A major symptom of the disease is an acute immune system failure, causing the patient to be susceptible to serious infections.
In clinical observations, patients who are seriously infected by mycobacterium may suffer constant high fever, generalized lymph node enlargement throughout the body, shingles (herpes zoster), severe pain in the bones and serious infection often occurred among patients with immunodeficiency.
When a patient with the disease is infected by fungus or mycobacterium, the autoantibody attacks the interferon-gamma in the immune system, making it unable to function properly and leading to worsened fungus or mycobacterium infection, but the pathogenesis had not been well understood.
Ku Cheng-lung (顧正崙), assistant professor at the university’s Graduate Institute of Clinical Medical Sciences and the research team leader, said the team discovered that many patients have a certain immune genotype often found in Taiwanese and Southeast Asians.
The team said there might be thousands or tens of thousands of people with the disease in Taiwan or Southeast Asian countries who have not been diagnosed yet.
“Because the protein structure of a certain part of the interferon-gamma is similar to that of fungus,” Ku said when people with this immune genotype are exposed to fungus, triggering anti-fungal antibodies, the antibodies attack the interferon-gamma, preventing it from working.
The team said current treatment for the disease — using antibiotics — has a limited effect on patients, and about two-thirds of the patient will relapse and continue to be seriously infected by fungus or mycobacterium.
Therefore, the team has developed a method to modify the structure of the interferon-gamma, so that it can avoid attacks by the antibody and allow it to regain proper immune function, and in vitro experiments have proved the method to be effective.
The discovery was published in the journal Nature Medicine.
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