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:

- 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").

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.
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