Immune Receptors Modulate Eosinophilic Functions in Viral Immunity


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Çıracı Muğan C.

6th European Congress of Immunology, İstanbul, Türkiye, 1 - 04 Eylül 2021, cilt.51, sa.513, ss.208

  • Yayın Türü: Bildiri / Özet Bildiri
  • Cilt numarası: 51
  • Doi Numarası: 10.1002/eji.202170200
  • Basıldığı Şehir: İstanbul
  • Basıldığı Ülke: Türkiye
  • Sayfa Sayıları: ss.208
  • İstanbul Teknik Üniversitesi Adresli: Evet

Özet

Eosinophils involvement in a broad spectrum of pathological conditions such as acute and chronic infections, cancer and thrombosis make them an interesting research topic. Despite their roles in parasitic infections, there is a growing body of evidence that eosinophils play roles in fungal, bacterial and viral infections. Studies on mouse and primary human eosinophils reveal the importance of eosinophils against viruses that cause airway inflammation such as influenza and respiratory syncial viruses. Moreover, recent studies on SARS-Cov-2 infection show eosinopenia in Covid-19 patients. However, the question how eosinophilic PRRs and immune receptors (IRs) are affected by viral infections remains elusive. Thus, the aim of this study is to elucidate the regulation of eosinophilic functions in antiviral immunity by measuring the production of  matrix metalloproteinases, eosinophil cationic protein, eosinophil-derived neurotoxin.

Initially, human eosinophilic Eol-1 cells were stimulated with various viral stimuli such as Poly I:C, R848, ssRNA40. The mRNA levels of PRRs, IRs, ECP and EDN were determined by QPCR and protein levels of TLR3, TLR7, TLR8, CARD9 were measured by western blotting. Additionally, we determined the MMP2 and MMP9 enzyme activities by gelatin zymography in response to viral stimulants. Of all the stimuli we tested, ssRNA40 was the most potent in inducing the mRNA expressions of TLR-3, TLR-7, TLR-8, CD147, CARD9, ECP, EDN, FcεR1a and FcεR2. Interestinly, CARD9 which is an key receptor for fungi infections was significantly elevated after treatment with TLR7/8 ligands, suggesting a primary role for TLR7 and 8 rather than TLR3 in viral defence by eosinophils.