Actinic prurigo is a long-lasting photosensitivity condition that is more commonly found among Amerindians and Latin American mestizos. It is strongly linked to the human leukocyte antigen DR4, particularly the DRB1*0407 subtype. Our company is well-equipped to address your drug and therapy development requirements in Actinic Prurigo therapy.
Introduction to Actinic Prurigo
Actinic prurigo is a rare, chronic photodermatosis characterized by intensely itchy papules, plaques, and nodules on sun-exposed skin. It is more prevalent in individuals of Latin American and American Indian descent, particularly those living at high altitudes. The condition affects about 0-5% of individuals in photodermatology clinics, with higher rates in Mexico, where it ranges from 3.5-5%. Women are more frequently affected than men, especially in adult-onset cases.
Pathogenesis of Actinic Prurigo
The pathogenesis of actinic prurigo (AP) involves a type IV hypersensitivity reaction to ultraviolet (UV) radiation. Genetic factors play a significant role, particularly the HLA-DRB1*0407 allele, which is common in affected populations. UV exposure triggers an immune response involving Th1 and Th2 pathways, leading to the release of cytokines like TNF-α, IL-5, and IL-4. This causes an inflammatory reaction characterized by the infiltration of T and B lymphocytes, eosinophils, and mast cells.
Fig. 1 Pathogenesis of Actinic Prurigo. (Vega Memije, M.E.,
et al., 2017)
Diagnosis Development of Actinic Prurigo
- Immunohistochemistry: Advanced techniques such as immunohistochemistry can further differentiate AP from other photodermatoses. The presence of specific immune cells, such as CD4+ and CD8+ T lymphocytes, and markers like TNF-α in keratinocytes, are indicative of AP.
- Genetic Testing: Given the strong association with the HLA-DRB1*0407 allele, genetic testing can support the diagnosis, particularly in populations with a high prevalence of this genetic marker, such as Native Americans and certain Latino groups.
Therapy Development of Actinic Prurigo
Small Molecule Drugs
Small molecule drugs are often used first due to their ability to modulate immune responses and reduce inflammation. Thalidomide reduces TNF-α production, helping severe cases. Hydroxychloroquine, an antimalarial, reduces inflammation triggered by UV radiation.
Cell Therapies
Cell therapies are in early development but show promise. Mesenchymal Stem Cells (MSCs) have anti-inflammatory properties and may reduce chronic inflammation. T Regulatory Cells (Tregs) help maintain immune tolerance and could control abnormal immune responses in actinic prurigo.
Gene Therapies
Gene therapies are experimental but offer potential. CRISPR/Cas9 can edit genes like HLA-DRB1*0407 to prevent abnormal immune responses. Gene Silencing Techniques, such as RNA interference, target overactive inflammatory genes.
Monoclonal Antibodies
Monoclonal antibodies target specific immune components to block inflammation. Dupilumab inhibits IL-4 and IL-13 signaling, reducing symptoms. Ustekinumab targets IL-12 and IL-23 to modulate immune responses.
Our Services
Our company embraces a partnership-driven approach. We work closely with clients to develop customized, innovative Actinic Prurigo therapy strategies and provide strong support throughout the process.
Platforms of Actinic Prurigo Therapy Development
We possess established expertise in developing and using animal models that accurately replicate the disease characteristics and therapeutic responses. These models allow us to assess the safety and efficacy of potential therapies.
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Non-Genetically Engineering Models |
| We offer a variety of models tailored to specific research needs related to Actinic Prurigo. These models enable researchers to simulate and investigate the complex biological processes involved in Actinic Prurigo. |
| Optional Models |
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- PDT-Induced Prurigo Model
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| Genetically Engineered Models |
| Our proficiency in genetic engineering techniques enables us to create precise and reliable models that replicate the genetic alterations seen in Actinic Prurigo. |
| Optional Models |
- IL-4 Knockout Mice Model
- Human HLA-DR4 Transgenic Mice Model
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- TNF-α Knockout Mice Model
- IL-13 Overexpressing Transgenic Mice Model
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| Optional Species |
Mice, Rats, Non-human primates, Others |
Additionally, we can offer other comprehensive Animal models services that focus on specific signaling pathways and molecular targets.
If our services interest you, please contact us at your earliest convenience for more details.
References
- Vega Memije, M.E., et al., "Actinic prurigo as a hypersensitivity reaction type 4." Int J Dermatol, (2017). 56(6): p. e135-e136.
- Sitek, J.C., "Actinic Prurigo in Scandinavian Adolescent Successfully Treated with Cyclosporine A." Dermatol Reports, (2017). 9(1): p. 7050.
All of our services and products are intended for preclinical research use
only and cannot be used to diagnose, treat or manage patients.
