Alopecia areata (AA) is an autoimmune condition where the immune system mistakenly attacks hair follicles, leading to hair loss. This can affect the scalp, eyebrows, eyelashes, or any other hair-bearing area of the body. Specialized drug and therapy development services are crucial to advancing AA research. Our company is fully equipped to meet your drug and therapy development needs for AA therapy.
Introduction to Alopecia Areata
Alopecia areata is a chronic autoimmune skin condition that causes non-scarring hair loss, affecting approximately 0.1% of the global population, with a lifetime incidence of about 2%. While it can occur at any age, it is most commonly diagnosed between ages 30 and 40. The condition impacts both males and females equally, although adult females have a slightly higher diagnosis rate.
Pathogenesis of Alopecia Areata
The pathogenesis of alopecia areata involves an abnormal immune response in which T cells aggregate around and attack hair follicles, leading to inflammation and disrupted follicle function. This autoimmune reaction is thought to result from a loss of immune privilege within the hair follicle, causing its destruction. Additionally, inflammatory pathways become activated, enhancing antigen presentation by follicular cells and triggering T cell-mediated damage to the follicles.
Fig. 1 In alopecia areata, CD8
+ T cells produce interferon-gamma (IFN-g), which signals viaJanus kinases 1 (JAK1) and JAK2 to enhance production of interleukin-15 (IL-15). (Strazzulla, L.C.,
et al., 2018)
Biomakers Development of Alopecia Areata
Scientists researching Alopecia Areata have identified several potential biomarkers.
- Cytokines and Chemokines: Monocyte Chemoattractant Protein (MCP), specifically MCP-1 (CCL2), is a cytokine found at elevated levels in individuals with Alopecia Areata. This increase is associated with inflammation and autoimmune responses related to the condition.
- Immune Cell Markers: In individuals with Alopecia Areata, abnormal expression levels of NKG2D receptors and their ligands around the hair follicles suggest that immune cells recognize these ligands and attack the hair follicles.
Therapy Development of Alopecia Areata
Small Molecule Drugs
Small molecule drugs such as JAK inhibitors (e.g., ruxolitinib and tofacitinib) have shown promise in clinical trials by blocking pathways that lead to the activation of immune cells and the attack on hair follicles, sometimes resulting in rapid hair regrowth.
Cell Therapies
Cell therapies include the use of regulatory T cells (Tregs) to restore immune balance and prevent attacks on hair follicles, as well as stem cell therapy, which aims to regenerate damaged hair follicles by introducing cells that can differentiate into hair-producing structures.
Gene Therapies
Gene therapies, though still in the experimental stage, include tools like CRISPR/Cas9 to potentially correct immune dysfunctions at the genetic level and techniques such as RNA interference (RNAi) to silence genes involved in AA, thereby reducing the expression of proteins that cause hair loss.
Monoclonal Antibodies
Monoclonal antibodies, such as Ustekinumab and Secukinumab, are engineered to target specific antigens. They focus on cytokines involved in inflammatory responses, like interleukin-12, interleukin-23, and IL-17A, aiming to reduce the inflammation that disrupts hair follicle function.
Our Services
Our company adopts a partnership-driven approach. We collaborate closely with clients to craft tailored, innovative Alopecia Areata therapy strategies and ensure robust support throughout the process.
Platforms of Alopecia Areata Therapy Development
We have established expertise in developing and utilizing relevant animal models that closely mimic the disease characteristics and response to therapy. These models enable us to evaluate the safety and efficacy of potential therapies.
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Non-Genetically Engineering Models |
| We provide diverse model choices customized to meet specific research needs related to Alopecia Areata. These models allow researchers to simulate and study the complex biological processes associated with Alopecia Areata. |
| Physical/Chemical Induced Model |
| Optional Models |
- DNCB (Dinitrochlorobenzene) Induced Model
- Ultrasonic Stress Induced Model
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- SADBE (Squaric Acid Dibutylester) Induced Model
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| Xenograft Models |
| Optional Models |
- Human Immune Cell Transfer Model
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| Genetically Engineered Models |
| Our expertise in genetic engineering techniques allows us to generate accurate and reliable models that recapitulate the genetic alterations observed in human Alopecia Areata. |
| Optional Models |
- HLA-DQ8 Transgenic Mice Model
- IL-2 Overexpression Mice Model
- Keratin-14 (K14) NF-kB Transgenic Mice Model
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- IFN-γ Transgenic Mice Model
- Rag-1 Knockout Mice Model
- Foxp3 Knockout Mice Model
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| Optional Species |
Mice, Rats, Non-human primates, Others |
In addition to these models, our comprehensive services encompass other models that target specific signaling pathways and molecular targets.
If our services align with your goals, please contact us for more details.
References
- Strazzulla, L.C., et al., "Alopecia areata: Disease characteristics, clinical evaluation, and new perspectives on pathogenesis." J Am Acad Dermatol, (2018). 78(1): p. 1-12.
- Sterkens, A., et al., "Alopecia areata: a review on diagnosis, immunological etiopathogenesis and treatment options." Clin Exp Med, (2021). 21(2): p. 215-230.
All of our services and products are intended for preclinical research use
only and cannot be used to diagnose, treat or manage patients.
