Dual nature of T-cell-epithelium interaction in chronic rhinosinusitis: activation then apoptotic death

T-cell infiltration of submucosa is observed in chronic rhinosinusitis (CRS). This T-cell infiltration leads to release of proinflammatory cytokines leading to epithelial activation.


Left-sided maxillar sinusitis (absence of the air transparency of left maxillar sinus). Image source: Wikipedia, public domain.

Sinus epithelial cells from patients with CRS were at an activated state with upregulated expression of:

- HLA-DR
- IFN-gamma-inducible protein 10
- monokine induced by IFN-gamma
- TNF-related apoptosis-inducing ligand (TRAIL)

The expressions of HLA-DR, TRAIL, and TNF receptor 2 were induced by IFN-gamma.

Epithelial cells started to undergo apoptosis 48 hours after IFN-gamma stimulation when the transcription of proinflammatory cytokines and chemokines decreased to initial levels.

The factors for apoptosis were T(H)1 cells and IFN-gamma.

Apoptosis was enhanced by Fas-Fas-ligand and TRAIL-TRAIL receptor 2 interactions.


Fas death domain (TNF receptor superfamily, member 6). Image source: Wikipedia, public domain.


This video describes the process by which apoptosis is activated by T cells. This video is from: Janeway's Immunobiology, 7th Edition Murphy, Travers, & Walport. Source: Garland Science.

Epithelial cell interaction with activated T cells is a biphasic phenomenon in CRS:

1. Initially T cells lead to activation and induction of proinflammatory functions of epithelial cells.

2. Apoptotic death ("exhausted cells die").

References:
Basinski TM, Holzmann D, Eiwegger T, Zimmermann M, Klunker S, Meyer N, Schmid-Grendelmeier P, Jutel M, Akdis CA. Dual nature of T-cell-epithelium interaction in chronic rhinosinusitis. J Allergy Clin Immunol. 2009 Jun 10.
Sinusitis: A Short Review