All
  • All
  • Insight
  • Research Services
  • Preclinical CRO
  • Animal Resource Bank
CN
中文 English

Alopecia Areata Animal Model

Alopecia Areata Animal Model

Explore more

Alopecia areata
Skin-related disease models

On this page

Model Introduction

Model Introduction

Platform Service Advantages

Platform Service Advantages

Model Construction

Model Construction

Publish an article

View more

Alopecia areata

Introduction to AA Animal Models

Alopecia areata (AA) is an autoimmune disorder that targets hair follicles, characterized primarily by focal or diffuse hair loss; in severe cases, it may progress to total alopecia or universal alopecia. Its pathogenesis is closely linked to the disruption of hair follicle immune privilege, aberrant activation of T lymphocytes, and dysregulation of multiple inflammatory cytokines. Animal models typically employ C3H/HeJ spontaneous AA mice, skin graft–induced AA models, or adoptive transfer models, which can recapitulate hallmark pathological features such as hair shedding, perifollicular lymphocytic infiltration, and premature termination of the anagen phase. These models effectively mimic the immunopathological processes observed in human alopecia areata.

Advantages of Aniphe BioLab’s AA Animal Model Platform Services

Aniphe BioLab has established a well‑established animal model platform for alopecia areata (AA), providing robust and reliable preclinical support for research into the mechanisms of autoimmune hair loss and the development of innovative therapies.

Comprehensive model coverage

Model resources are mature.

It supports the establishment of classic AA models, such as the C3H/HeJ spontaneous alopecia areata model and the skin graft‑induced model.

Standardization of the modeling process

Model phenotype stability

It can stably recapitulate the typical features of alopecia areata, including hair loss, follicular regression, and immune cell infiltration.

Multidimensional Evaluation System

The evaluation system has been improved.

It encompasses multi-dimensional analyses, including hair removal area scoring, hair regrowth assessment, histopathological examination, and immunological assays.

Adapted for multi-cycle studies

One-stop service platform

We offer end-to-end services, including model development, dosing regimen design, sample analysis, pathological assessment, and statistical data analysis.

Modeling cycle

5–16 weeks

1  Laboratory animals

C3H/HeJ mice, NSG mice

1  Positive drug

Primarily consisting of JAK inhibitors (tofacitinib, ruxolitinib), cyclosporine A, and glucocorticoids.

1  Application areas

Applications are focused on research into autoimmune mechanisms, evaluation of JAK‑pathway inhibitors, hair follicle regeneration, and optimization of immunotherapy, among other areas.

AA Animal Model Construction

01 Spontaneous alopecia areata model in C3H/HeJ mice

C3H/HeJ mice are one of the most widely used animal models of alopecia areata (AA). With advancing age, this strain spontaneously develops hallmark pathological features of AA, including hair loss, follicular atrophy, and extensive perifollicular infiltration by CD4⁺ and CD8⁺ T cells. Focal hair loss typically emerges between 6 and 12 months of age and may progress to diffuse alopecia. As an autoimmunity‑driven model that requires no exogenous induction, it closely mimics the autoimmune pathogenesis of human AA and is extensively employed in studies of AA pathogenesis and immunomodulatory therapeutics.

02 Human hair follicle transplantation + CD8⁺ T cell–induced model

Using immunodeficient mice (such as NSG mice) as recipients, human hair follicle tissue is transplanted subcutaneously. Once the follicles have established stable engraftment, ex vivo‑activated human CD8⁺ T cells or patient‑derived immune cells are injected. These CD8⁺ T cells can target the hair follicle architecture, disrupt its immune‑privileged status, and induce the follicles to enter the catagen phase, resulting in alopecia and inflammatory cell infiltration—hallmark features of alopecia areata. This model faithfully recapitulates the key immunopathological processes of human‑derived alopecia areata, making it well suited for preclinical evaluation of humanized therapeutic strategies, mechanisms of immune regulation, and novel targeted agents.

 

Treatment data for tofacitinib and ruxolitinib

Tofacitinib and ruxolitinib, as classic JAK‑pathway‑positive agents in alopecia areata models, significantly promote hair regrowth in C3H/HeJ mice with alopecia areata, reduce the infiltration of CD8⁺NKG2D⁺ cytotoxic T cells, and ameliorate the local immune‑inflammatory milieu within hair follicles. This study confirms the pivotal role of the JAK‑STAT signaling axis in the pathogenesis and progression of alopecia areata, providing a reliable positive‑control reference for evaluating the efficacy of therapeutic agents in this condition.

 

 

Specific literature references: Alopecia areata is driven by cytotoxic T lymphocytes and is reversed by JAK inhibition.