Immunology

The Institute examines the pathogenesis of bronchial asthma and abnormalities of the immune system and studies the defense mechanism against human parasites and viruses and innate immunity related research including TLR. The Institute also focuses on developing treatments for allergic and immune diseases using immunomodulatory functions such as DNA vaccination and immunostimulatory sequence oligonucleotides. In addition, the Institute analyzes and identifies the causes of allergic and immune diseases at the genetic level and analyzes the effects of the environment, especially air pollutants, on human respiratory tissue.
It identifies candidate genes involved in bronchial asthma and allergic diseases, reports significant genes through correlation analysis, and participates in advancing the era of personalized therapy through pharmacogenetics research on respiratory drugs.
Immunology Seminar: The Institute holds academic conferences and advanced lectures with invited speakers from home and abroad who are actively researching in the field of allergy and immunology. In particular, this immunology seminar is open to research institutes as well as to those interested in this field. The seminar is not only a place for academic exchanges in allergy and clinical immunology, but also contributes to the promotion of building research networks and joint research.
1. Effect of macrophage modulation on asthma and Target Molecule Discovery
The pathogenesis of asthma is based on excessive Th2 responses. Imbalance between Th1, Th2, and Th17 cells with unregulated Treg cells also have been reported to play an important role in aggravation of asthma. Recent studies however, have revealed that innate immune cells and innate lymphoid cells(ILCs) are also deeply involved in the pathogenesis of asthma.
Among many different innate immune cells, we are focusing on macrophages and asthmatic phenotypes differ depending on their modulations. Through studying differences in activation and subtype modulation of macrophages in various asthma models, The Institute of Allergy and Clinical Immunology aims to understand the mechanisms of pathogenesis of asthma and to define target biomarkers for treatment.
2. Therapeutics for Asthma using Microbiomes
Hygiene Hypothesis, which has been considered to be highly associated with pathogenesis of asthma along in microbiome researches, is yet confined to investigating the correlation between asthma and microbiomes. We are taking further steps to reveal interrelations and cause-and-effect relationship between asthma and microbial changes using various types of symbiotic bacteria.
In addition, bacterial infections leading to aggravation of asthma are known to be accompanied by exposure to lipopolysaccharides, a component of the bacterial cell wall. Because lipopolysaccharides are endotoxins that induce immune responses, we are conducting researches that help define subtypes of asthma based on immune response that vary depending on concentration and duration of exposure to lipopolysaccharides.
3. Stem Cell Therapy for Asthma
Persistent attention for diseases with no known cure is driving stem cell research to fast expanding markets worldwide, yet current stem cell researches are limited to revealing their immunomodulatory effects. The Institute of Allergy and Clinical Immunology aims to further develop researches to discovering clinical therapeutics for asthma, an incurable airway inflammation.
Mesenchymal stem cells(MSCs), multipotent stromal cells that can differentiate into variety of cell types, are known to have great capacity for self-renewal and are relatively easy to be handled in laboratory settings. By applying MSCs to diverse murine models of acute and chronic asthma induced by different types of allergens, we seek to discover biomakers that link to pathogenesis and immunomechanism of asthma. Additionally established pulmonary fibrosis model, which portraits one of the symptoms of patients with severe asthma, is used to evaluate anti-fibrotic effects of MSCs along with their anti-inflammatory effects.