"Factors Worsening Refractory Lupus Due to Immune Cell 'Mitochondria' Dysfunction"

Seoul St. Mary's Hospital's Park Seonghwan and Catholic University Medical School's Professor Cho Mira Team
Regulation of 'CRIP1' in Mitochondria
New Therapeutic Strategy for Autoimmune Diseases Identified

Professor Seonghwan Park (left), Department of Rheumatology, Seoul St. Mary's Hospital, Catholic University, and Professor Mira Cho, College of Medicine.

[Asia Economy Reporter Lee Gwan-joo] A study conducted by Korean researchers has revealed that mitochondrial dysfunction in immune cells exacerbates lupus, a representative autoimmune disease.

The research team, led by Professor Park Sung-hwan of the Rheumatology Department at Seoul St. Mary's Hospital, The Catholic University of Korea (co-corresponding author), Professor Cho Mira of the Department of Medical Life Sciences at the College of Medicine (co-corresponding author), and Research Professor Park Jin-sil (first author), announced on the 25th that they clarified the impact of mitochondrial dysfunction in B lymphocytes on lupus development using an animal model (mouse) selectively deficient in the 'CRIP1' protein in B lymphocytes.

Mitochondria are intracellular organelles responsible for cellular energy production. Mitochondrial dysfunction is closely related to various diseases, including aging, cancer, and diabetes, and is reported to play a key role in the development of autoimmune diseases. CRIP1 mainly exists in the mitochondrial inner membrane and functions to insert proteins produced in mitochondria into the mitochondrial inner membrane.

The study found that the animal model selectively deficient in CRIP1 in B lymphocytes showed an increase in serum anti-double stranded DNA antibodies, a target antibody of lupus, as they aged, and inflammation in kidney tissues worsened.

The research team observed improvement of the disease when CRIP1 gene therapy was applied to lupus disease animal models, and confirmed that overexpression of CRIP1 in peripheral blood mononuclear cells of lupus patients reduced the production of interleukin 17, known as an inflammatory cytokine.

Professor Park said, “Lupus is a disease with a thousand faces, as each patient presents different symptoms, making diagnosis difficult. If treatment is delayed or neglected, the disease can invade and worsen major organs such as the kidneys, nervous system, lungs, and heart. Therefore, rapid and accurate diagnosis and treatment by experts are necessary. Through this study, gene-targeted therapy related to mitochondrial function shows great potential as a next-generation major therapeutic candidate.”

This study was published in the July issue of 'Arthritis & Rheumatology,' the official journal of the American College of Rheumatology, the world's leading organization of rheumatology experts and the top authority in rheumatic diseases.

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