The study was funded by
@usisraelbsf
@IsraelAcademy
@azrielifdn
@AstraZeneca

8/8

🧬 RNA-seq analysis of esophageal tissue revealed that TSLP controls the expression of IL-13-dependent genes central to human EoE:
🧪 Eotaxins, IL-19, FLG, KLK5, IL36RN, IL1R2
📌 TSLP shapes barrier integrity, IL-1 signaling, and epithelial differentiation.
7/8

🧪 Key finding #2
IL-33 plays a more limited role.
Il33⁻/⁻ mice showed reduced eosinophilia, but no impact on tissue remodeling suggesting non-redundant roles for TSLP and IL-33 in EoE.
6/8

🧪 Key finding #1
TSLP is essential for EoE pathogenesis.
Crlf2⁻/⁻ mice were nearly completely protected from developing EoE.
Neutralizing TSLP reduced:
✅ Eosinophilia
✅ Basal cell proliferation
✅ Vascularization
✅ Lamina propria thickening
5/8

To answer this, we used genetic and antibody-based approaches in a validated mouse model of EoE (onlinelibrary.wiley.com/doi/10.1111/...).
We studied WT, Il33⁻/⁻, and Crlf2⁻/⁻ (TSLP receptor knockout) mice, and applied neutralizing antibodies to TSLP or IL-5.
4/8

Two epithelial-derived cytokines TSLP and IL-33 have been implicated in allergic diseases.
But what is their role in EoE?
And are they redundant or functionally distinct in driving this disease?
#Immunology #EoE #Eosinophils
3/8

🔬 EoE is a chronic food allergy-induced inflammation of the esophagus that is currently on the rise. It is characterized by eosinophilia, basal cell hyperplasia, and tissue remodeling. It causes swallowing difficulties, pain, and growth delay. @EosinophilSoc #Allergy
2/8

Thanks Shai