Photo Credit: Nemes Laszlo

The following is a summary of “Expansion of multiple CD4+ T cell lineages in lymphocytic variant hypereosinophilic syndrome,” published in the May 2025 issue of Journal of Allergy and Clinical Immunology by Anderson et al. 

Lymphocytic variant hypereosinophilic syndrome (LHES) was characterized by hypereosinophilia, aberrant T helper type 2 (Th2) lymphocyte populations, and diverse clinical features. Disease pathogenesis was previously attributed to IL–5–mediated eosinophilia.   

Researchers conducted a retrospective study to describe the surface phenotypes and cytokine profiles of aberrant lymphocyte populations in patients with Lymphocytic variant hypereosinophilic syndrome.   

They performed multiparameter flow cytometry to examine lymphocytes in both whole blood and cryopreserved peripheral blood mononuclear cells (PBMCs) from a total of 42 patients diagnosed with LHES, including both untreated and treated individuals.  

The results showed that surface receptor analysis in 22 untreated patients with LHES, including 8 with episodic angioedema with eosinophilia (EAE), confirmed that aberrant CD4⁺ T cells displayed a Th2 memory profile and CCR8 emerged as a predominant surface marker, unaffected by treatment or processing. Serum levels of CCL1, the CCR8 ligand, were higher in LHES compared to other hypereosinophilic syndrome (HES) variants. Many patients with CD3^lo CD4⁺ LHES showed increased Foxp3⁺ Helios⁺ CCR8⁺ regulatory T cell populations, which correlated with CD3^lo CD4⁺ cell expansion.  

Investigators concluded that these data provided further evidence for the direct involvement of aberrant T cell populations in the pathogenesis of LHES and supported further exploration of T cell-directed therapies. 

Source: jacionline.org/article/S0091-6749(25)00509-3/abstract