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Programmed cell death‐1 expression correlates with disease severity and IL‐5 in chronic rhinosinusitis with nasal polyps
Author(s) -
Kortekaas Krohn I.,
Bobic S.,
Dooley J.,
Lan F.,
Zhang N.,
Bachert C.,
Steelant B.,
Bullens D. M.,
Liston A.,
Ceuppens J. L.,
Seys S. F.,
Hellings P. W.
Publication year - 2017
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/all.13136
Subject(s) - nasal polyps , medicine , immunohistochemistry , pathology , flow cytometry , immunology
Background Programmed cell death‐1 (PD‐1) is a negative regulator of T‐cell responses. Expression of PD‐1 and its ligands PD‐L1 and PD‐L2 in chronic rhinosinusitis with nasal polyps (CRSwNP) is poorly studied. Methods Expression of PD‐1, PD‐L1, PD‐L2, TGF‐β, IL‐5, and IL‐10 mRNA was measured by real‐time quantitative PCR on tissue homogenates of patients with CRSwNP ( n = 21) and healthy controls ( n = 21) and on primary epithelial cells. Disease severity was scored using the Lund–Mackay scores of maxillofacial computed tomography (CT) scans. Expression of PD‐1 and PD‐L1/L2 was evaluated at the cellular and tissue levels ( n = 6) by flow cytometry and immunohistochemistry. Results Programmed cell death‐1 mRNA expression was increased in tissue homogenates from patients with CRSwNP compared with controls, irrespective of the atopy status. Importantly, expression of PD‐1 correlated with the total CT scan scores ( r = 0.5, P = 0.02). Additionally, a significant association was found between PD‐1 mRNA and expression of IL‐5 mRNA in control nasal tissue ( r = 0.95, P < 0.0001) and in CRSwNP ( r = 0.63, P = 0.002). PD‐1 was expressed on different subsets of T cells and CD11b − dendritic cells. Both PD‐1 and its ligands were expressed on primary epithelial cells from control nasal tissue and nasal polyp tissue. Conclusions Higher PD‐1 expression was found in CRSwNP than in nasal tissue from controls. This was associated with disease severity and tissue IL‐5 expression but unrelated to the patients' atopy status.