The relationship between B7 homologous 1 with interleukin-4, interleukin-17 and interferon gamma in patients with allergic rhinitis

ABSTRACT

Background: The etiology of allergic rhinitis includes an increase in cytokine levels, including IL- 4, IL-13, IL-17, and reduction in B7 homologous 1 (B7-H1) or programmed cell death-1 ligand-1 (PD-L1), a new member of the CD28: B7 stimulant molecule family. The aim of this study was to determine the relationship between cytokines and PD-L1.

Methods: In this experimental study, 80 patients with allergic rhinitis were enrolled according to inclusion and exclusion criteria. The severity and stage of the disease were determined by a specialist physician. A 5 cc venous blood sample was collected from the patients. IL-4, IL-17, INFγ and PD-L1 were measured using ELISA technique.

Results: There was a significant correlation between SPD-L1 and INFγ, IL-4 and IL-17 in allergic rhinitis patients (P < 0.05). Statistical analysis based on the severity of the disease (Mild, Moderate and Severe) showed a significant positive correlation between the SPD-L1 and INFγ in all three levels (P < 0.001). There was also a significant negative correlation between SPD-L1 and two cytokines IL-4 and IL-17 (P < 0.001).

Conclusion: PD-L1 may have a protective role against allergic rhinitis, although the precise mechanism requires further detailed studies.

KEYWORDS:

• B7 homologous 1
• Interleukin-4
• Interleukin-17
• Interferon gamma
• allergic rhinitis

Acknowledgments

The study was approved by Kurdistan University of Medical Sciences (No 1396.95).

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

The study was funded by Kurdistan University of Medical Sciences (No 1396.95).