A research group at Chiba University Graduate School of Medicine has elucidated the mechanism of action of sublingual immunotherapy for cedar pollinosis.A new molecule called masculin was confirmed, and it is expected to be used as a biomarker for sublingual immunotherapy and to improve the same therapy.
Although the number of patients with allergic rhinitis tends to increase, general oral administration of antihistamines and nasal steroid treatment are symptomatic treatments, not curative treatments.Sublingual immunotherapy, in which immune tolerance is acquired by repeated exposure to low-concentration antigens, is the only treatment that is expected to improve the constitution of cedar pollinosis. Due to unknowns, development is not progressing.
The research group has been researching memory T cells (Tpath2 cells) that are the etiology of allergic diseases.In this study, a total of 14 blood samples were compared before and after sublingual immunotherapy from XNUMX subjects using "single-cell analysis," which comprehensively analyzes the genes of individual cells.
As a result, it was found that Tpath2 cells, which produce allergy-related cytokines (white blood cells and cell-to-cell messengers) in response to cedar pollen, decreased, and Th2 cells (TransTh2 cells) and regulatory T cells (Treg cells) that suppress inflammation.We also found the possibility that Tpath2 cells differentiate into Treg cells through changes to TransTh2 cells.Furthermore, it was found that this change was due to the expression of masculin (MSC), a factor that suppresses the function of Th2 cells and promotes their differentiation into Treg cells.
Masculin can be used as a biomarker for sublingual immunotherapy, and observation of changes is expected to improve sublingual immunotherapy.It is also possible to apply it to other allergic diseases.In the future, we will pursue the changes and significance of this masculine and promote the development of new immunotherapy.
Paper information:[Journal of Allergy and Clinical Immunology] Single-cell immunoprofiling after immunotherapy for allergic rhinitis reveals functional suppression of pathogenic TH2 cells and clonal conversion