Alopecia Areata

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Alopecia Areata (AA) is an (auto-) inflammatory hair loss disorder with approximately 2% of the global population affected over their lifetime.

AA is driven by Th1-mediated responses that impact the hair follicle bulb. CD8+ T-cells attack anagen hair follicles, releasing pro-inflammatory agents such as IFNγ. This triggers peri- and intrafollicular inflammation, leading to the breakdown of the hair follicle’s immune privilege. This breakdown is marked by an increase in major histocompatibility complex class I and II expression, suppression of immune privilege guardians, and elevated levels of pro-inflammatory molecules. The resulting inflammation recruits more immune cells, causing hair follicle damage, dystrophy, and premature catagen induction.

Recently, the FDA approved a JAK1/JAK2 inhibitor and a JAK3/TEC inhibitor as oral treatments for AA. While these therapies have shown promise, they are not effective in all patients. Additionally, some patients experience hair loss recurrence after discontinuing treatment, reduced responsiveness over time, or severe long-term side effects due to the broad immunosuppressive nature of these drugs.

To address these challenges, there is a pressing need to develop more targeted, locally-administered treatments that reduce side effects and lower relapse rates.

At QIMA Life Sciences, we support our clients in drug discovery and development by providing advanced solutions for both preclinical and clinical stages.

Interested in learning how we can support your drug discovery and development?

Learn more below.

Related Publications

SELECTED PUBLICATIONS ON ALOPECIA AREATA

Involvement of ILC1-like innate lymphocytes in human autoimmunity: lessons from alopecia areata

Downregulation of pathogenic MICA-NKG2D interactions as a novel strategy in alopecia areata management: a new rationale for adjunct statin therapy?

Mouse Models of Alopecia Areata: C3H/HeJ Mice Versus the Humanized AA Mouse Model

Pro-inflammatory Vδ1 + T-cells infiltrates are present in and around the hair bulbs of non-lesional and lesional alopecia areata hair follicles

Hair follicle immune privilege and its collapse in alopecia areata

>> Check the full list HERE.

Conference Contributions

We share our research on dermatology and trichology through international conferences and publications, contributing to the advancement of research in these fields.

>> Check our past contributions HERE.

Preclinical Research Solutions for Alopecia Areata

IN VITRO MODELS

  • Experimentally-induced AA-like phenotype in primary isolated ORSK (outer root sheath keratinocytes)
  • Immune cells from healthy donors or AA patients

EX VIVO MODELS

  • Human scalp skin explants
  • Healthy or diseased human hair follicle organ culture
  • Experimentally-induced hair follicle immune privilege collapse
  • Co-culture of human hair follicles and human blood- or skin-derived immune cells
  • Organ culture of lesional and non-lesional skin from AA patients

IN VIVO MODELS

  • Humanized mouse model of AA (created through a collaboration with Prof. Amos Gilhar, Skin Research Laboratory, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel)

Clinical Research Solutions for Alopecia Areata

BIOANALYSIS OF CLINICAL SAMPLES

  • Sample collection (scalp skin biopsies)
  • Analysis and quantification of cellular components (proteins, lipids) via analytical chemistry
  • AA biomarker analysis in tissue, blood and non-invasive collected samples

CLINICAL IMAGING

  • Image capture
  • Image analysis of AA lesions

CLINICAL TRIALS

  • Clinical study implementation
  • Clinical study performance
  • Data management
  • Data analysis

Alopecia Areata Study Examples

IFN-γ UPREGULATES IMMUNE PRIVILEGE MARKER EXPRESSION IN KERATINOCYTES IN VITRO

Test: Expression of MHC class I and -II

Method: Immunofluorescence staining

Model: Outer Root Sheath Keratinocytes (ORSK) in vitro

Interpretation of results: Stimulation with IFN-γ induces the expression of the immune privilege markers MHC class I and II in ORSK.

TOFACITINIB PREVENTS IFN-γ INDUCED PREMATURE CATAGEN INDUCTION IN HEALTHY HUMAN HAIR FOLLICLES EX VIVO

Test: Microscopic analysis of hair cycle stages

Method: Quantitative (immuno-)histomorphometry

Model: Healthy human hair follicle organ culture ex vivo

Interpretation of results: Stimulation with IFN-γ induces premature catagen development, a hallmark of AA, which is prevented by addition of the JAK inhibitor Tofacitinib.

LESIONAL AA SCALP SKIN IS CHARACTERIZD BY HIGHER NUMBERS OF CD3+ T CELLS

Test: Analysis of immune cells

Method: Immunofluorescence staining

Model: Non-lesional and lesional AA scalp skin organ culture ex vivo

Interpretation of results: The number of peri- and intrafollicular CD3+ T cells is significantly higher in lesional compared to non-lesional scalp skin, indicating an ongoing inflammatory response.

HAIR RE-GROWTH IS INDUCED BY DEXAMETHASONE AND MINOXIDIL IN THE HUMANIZED MOUSE MODEL OF AA

Test: Macroscopic analysis of hair re-growth

Method: Quantification of the number of hairs/graft

Model: Humanized mouse model of AA

Interpretation of results: Treatment of human, AA-induced scalp skin xenografted on SCID mice with a combination of Dexamethasone and Minoxidil efficiently induces hair re-growth.

VehicleIFNγ

At QIMA Life Sciences, we are committed to staying at the forefront of dermatology research by developing innovative approaches.

We offer smart solutions for studying alopecia areata using validated models at both preclinical and clinical stages, making us the perfect partner for your research.

Explore Our Models & Assays in Our Flyer

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alopecia aerata flyer

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SKIN & HAIR RESEARCH

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