Increased CD86 but not CD80 and PD-L1 expression on liver CD68+ cells during chronic HBV infection

Elias A. Said, Iman Al-Reesi, Marwa Al-Riyami, Khalid Al-Naamani, Shadia Al-Sinawi, Mohammed S. Al-Balushi, Crystal Y. Koh, Juma Z. Al-Busaidi, Mohamed A. Idris, Ali A. Al-Jabri

Research output: Contribution to journalArticlepeer-review

23 Citations (Scopus)


Background: The failure to establish potent anti-HBV T cell responses suggests the absence of an effective innate immune activation. Kupffer cells and liver-infiltrating monocytes/macrophages have an essential role in establishing anti-HBV responses. These cells express the costimulatory molecules CD80 and CD86. CD80 expression on antigen-presenting cells (APCs) induces Th1 cell differentiation, whereas CD86 expression drives the differentiation towards a Th2 profile. The relative expression of CD80, CD86 and PD-L1 on APCs, regulates T cell activation. Few studies investigated CD80 and CD86 expression on KCs and infiltrating monocytes/macrophages in HBV-infected liver and knowledge about the expression of PD-L1 on these cells is controversial. The expression of these molecules together in CD68+cells has not been explored in HBV-infected livers. Methods: Double staining immunohistochemistry was applied to liver biopsies of HBV-infected and control donors to explore CD80, CD86 and PD-L1 expression in the lobular and portal areas. Results: Chronic HBV infection was associated with increased CD68+CD86+ cell count and percentage in the lobular areas, and no changes in the count and percentage of CD68+CD80+ and CD68+PD-L1+ cells, compared to the control group. While CD68+CD80+ cell count in portal areas correlated with the fibrosis score, CD68+CD80+ cell percentage in lobular areas correlated with the inflammation grade. Conclusion: The upregulation of CD86 but not CD80 and PD-L1 on CD68+ cells in HBV-infected livers, suggests that these cells do not support the induction of potent Th1. Moreover, the expression of CD80 on CD68+ cells correlates with liver inflammation and fibrosis.

Original languageEnglish
Article numbere0158265
Pages (from-to)e0158265
JournalPLoS One
Issue number6
Publication statusPublished - Jun 2016

ASJC Scopus subject areas

  • General


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