Application of hair follicle immune homeostasis regulation strategy in treatment of alopecia diseases

By targeting and regulating the immune function of dendritic cells, and combining JAK kinase inhibitors and CGRP receptor agonists to exogenously supplement the CGRP pathway, the side effects and model limitations of existing alopecia areata treatments have been resolved, achieving effective hair growth and pigmentation effects and reliable animal model construction.

CN122140942APending Publication Date: 2026-06-05SHANGHAI FIRST PEOPLES HOSPITAL
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Patent Information

Application Number
CN202610100862.4
Authority / Receiving Office
CN · China
Patent Type
Applications(China)
Current Assignee / Owner
Filing Date
2026-01-23
Publication Date
2026-06-05

AI Technical Summary

Technical Problem

Among the existing treatments for alopecia areata, JAK kinase inhibitors are effective but have side effects, and the success rate of spontaneous animal models is low and the cost is high. They are also difficult to effectively target the collapse of the immune exemption in hair follicles, leading to poor treatment response or disease progression.

Method used

By targeting and regulating the immune function of dendritic cells, a combination of a JAK kinase inhibitor and a neuropeptide CGRP receptor agonist was used in conjunction with a spontaneous alopecia areata animal model to simulate the hair loss process of alopecia areata patients. Exogenous supplementation of the CGRP pathway negatively regulates the immune response of dendritic cells and improves hair follicle homeostasis.

Benefits of technology

This approach achieves enhanced hair growth and pigmentation while reducing side effects, providing a more effective treatment strategy for alopecia areata. It also establishes a stable and reliable spontaneous animal model to support drug screening and disease mechanism research.

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Abstract

The invention provides application of a hair follicle immune homeostasis regulation strategy in treatment of alopecia diseases. And identifying to obtain a group of alopecia areata pathological LAMP < 3 + > CCR7 < + > IL4I1 < + > DC3 dendritic cell subgroups. A spontaneous alopecia areata animal model constructed by driving conditional knockout of one of CGRP receptor compounds Calcrl by using a DC3 dendritic cell subset marker gene Il4i1 can be used for well simulating progressive and active alopecia of alopecia areata patients, forming stable alopecia patches and combining pathological changes such as hair follicle immune cell infiltration and the like; it is prompted that the CGRP signal deletion of the dendritic cell is an important cause of mediating systemic alopecia areata. Also disclosed are pharmaceutical compositions or kits for alleviating / treating alopecia, improving hair follicle homeostasis, or enhancing hair growth / black coloring (reducing white hair), comprising (a) a JAK kinase inhibitor, and (b) a neuropeptide CGRP or a receptor agonist thereof.
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