Innate Lymphoid Cell and Mast Cell Distributions in Chronic Rhinosinusitis Subtypes

Caroline J. Padro Dietz, PhD, Aravind Yadav, MD, Faramarz Ashoori, MD, Samer Fakhri, MD, Martin Citardi, MD, Amber U. Luong, MD, PhD

Author address: 

University of Texas Health Science Center at Houston, Houston, TX



Chronic rhinosinusitis (CRS) describes inflammatory diseases of the sinonasal mucosa and is subdivided into Th1-associated (CRS without nasal polyps (CRSsNP)) and Th2-associated diseases (CRS with NP (CRSwNP)) based on cytokine profiles (IFN-γ vs IL-5, respectively). Allergic fungal rhinosinusitis (AFRS) is a CRSwNP clinical subtype with fungal involvement. Compared to many human inflammatory diseases, CRS provides a unique opportunity to characterize local immune cell populations from tissue surgically removed as part of standard therapy. Innate lymphoid cells (ILCs) secrete cytokines characteristic of Th1 (ILC1), Th2 (ILC2) and Th17 (ILC3) cells. Understanding ILC subtype distribution may represent a novel target in CRS, specifically, and Th1- and Th2-driven diseases overall.



Sinonasal tissue was surgically obtained from CRSsNP (n=3), CRSwNP (n=7), and AFRS (n=4) patients. ILC1 (Lineage negative/CRTH2-/CD127+/CXCR3+), ILC2 (Lineage negative/CD127+/CRTH2+), and ILC3 (Lineage negative/CRTH2-/CD127+/NKp44+) populations from dissociated tissue were analyzed by flow cytometry and results are reported as a percentage of lymphocytes.



ILC1 percentage in CRSsNP (.53 +/- .18%) was slightly less than in CRSwNP (1.56 +/- .42%, p=.08) and AFRS (2.44 +/- 1.89%). The ILC2 percentage in CRSsNP (3.51 +/- 1.63%) was equivalent to CRSwNP (2.6 +/-.7%). ILC3 percentage in CRSwNP (.29 +/- .08%) was higher than in CRSsNP (.16 +/- .12%) and AFRS (.06 +/- .02%).



The mean percentages of ILC1 and ILC2 were similar among CRS subtypes. Notably, CRSwNP had wide percent distribution for all 3 ILC types not observed in CRSsNP and AFRS, mirroring its clinical heterogeneity. Finally, ILC3 presence in CRSwNP suggests a possible role in its pathophysiology.

abstract No: 

    • AAAAI 2015 (71st)