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Updated: Feb 8, 2026

Author Spotlight: Investigating the Pathophysiology of Eosinophilic Esophagitis
Published on: May 10, 2024
Differences in regulatory T cells between Churg-Strauss syndrome and chronic eosinophilic pneumonia with asthma
Naomi Tsurikisawa1, Hiroshi Saito, Takahiro Tsuburai
1Clinical Research Center for Allergy and Rheumatology, National Hospital Organization Sagamihara National Hospital, Kanagawa, Japan. n-tsurikisawa@sagamihara-hosp.gr.jp
Background:
Chronic eosinophilic pneumonia (CEP) with asthma precedes the onset of Churg-Strauss syndrome (CSS) in half of all patients with CSS. It is not known what determines whether patients with CEP after asthma will have CSS.
Objective:
We examined whether activation of regulatory T cells in patients with CEP inhibits CSS development and is otherwise involved in the mechanism of CSS disease.
Methods:
In patients with CSS (n = 38), CEP with asthma (n = 20), and general adult asthma (n = 108), we examined the number of CD4(+)CD25(+) T cells in peripheral blood, as well as levels of expression of the cytokines IL-2, IL-5, IL-10, and TGF-beta by CD4(+)CD25(+) T cells, CD4(+)CD25(-) T cells, or both.
Results:
At disease onset, patients with CSS, unlike patients with CEP, had significantly fewer CD4(+)CD25(+) T cells than patients with any step of asthma. CD4(+)CD25(+) T cells producing IL-10 were rarely detected in patients with CSS at disease onset or relapse, whereas the numbers of IL-10-producing T cells in patients with CEP were high at disease onset. There were fewer CD4(+)CD25(-) T cells producing IL-2 in patients with CSS before treatment than in patients with CEP at disease onset. The proportions of CD4(+)CD25(+) T cells producing IL-10 and CD4(+)CD25(-) T cells producing IL-2 in patients with CSS increased at remission.
Conclusions:
Maintenance of the numbers of regulatory T cells in patients with CEP with asthma might inhibit CSS development through the action of cytokines, such as IL-10 and IL-2, produced by CD4(+)CD25(+) or CD4(+)CD25(-) T cells. This might be part of a mechanism that influences progression and prognosis in these diseases.
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