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
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.
Leukocyte L1 Antigen Complex
Said, E. A., Al-Reesi, I., Al-Riyami, M., Al-Naamani, K., Al-Sinawi, S., Al-Balushi, M. S., ... Al-Jabri, A. A. (2016). Increased CD86 but Not CD80 and PD-L1 expression on liver CD68+ cells during chronic HBV infection. PLoS One, 11(6), [e0158265]. https://doi.org/10.1371/journal.pone.0158265
Increased CD86 but Not CD80 and PD-L1 expression on liver CD68+ cells during chronic HBV infection. / Said, Elias A.; Al-Reesi, Iman; Al-Riyami, Marwa; Al-Naamani, Khalid; Al-Sinawi, Shadia; Al-Balushi, Mohammed S.; Koh, Crystal Y.; Al-Busaidi, Juma Z.; Idris, Mohamed A.; Al-Jabri, Ali A.
Said, EA, Al-Reesi, I, Al-Riyami, M, Al-Naamani, K, Al-Sinawi, S, Al-Balushi, MS, Koh, CY, Al-Busaidi, JZ, Idris, MA & Al-Jabri, AA 2016, 'Increased CD86 but Not CD80 and PD-L1 expression on liver CD68+ cells during chronic HBV infection', PLoS One, vol. 11, no. 6, e0158265. https://doi.org/10.1371/journal.pone.0158265
Said EA, Al-Reesi I, Al-Riyami M, Al-Naamani K, Al-Sinawi S, Al-Balushi MS et al. Increased CD86 but Not CD80 and PD-L1 expression on liver CD68+ cells during chronic HBV infection. PLoS One. 2016 Jun 1;11(6). e0158265. https://doi.org/10.1371/journal.pone.0158265
Said, Elias A. ; Al-Reesi, Iman ; Al-Riyami, Marwa ; Al-Naamani, Khalid ; Al-Sinawi, Shadia ; Al-Balushi, Mohammed S. ; Koh, Crystal Y. ; Al-Busaidi, Juma Z. ; Idris, Mohamed A. ; Al-Jabri, Ali A. / Increased CD86 but Not CD80 and PD-L1 expression on liver CD68+ cells during chronic HBV infection. In: PLoS One. 2016 ; Vol. 11, No. 6.
@article{4a92cd81ad4844c69f9f93c21bea7281,
title = "Increased CD86 but Not CD80 and PD-L1 expression on liver CD68+ cells during chronic HBV infection",
abstract = "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.",
author = "Said, {Elias A.} and Iman Al-Reesi and Marwa Al-Riyami and Khalid Al-Naamani and Shadia Al-Sinawi and Al-Balushi, {Mohammed S.} and Koh, {Crystal Y.} and Al-Busaidi, {Juma Z.} and Idris, {Mohamed A.} and Al-Jabri, {Ali A.}",
T1 - Increased CD86 but Not CD80 and PD-L1 expression on liver CD68+ cells during chronic HBV infection
AU - Said, Elias A.
AU - Al-Reesi, Iman
AU - Al-Riyami, Marwa
AU - Al-Naamani, Khalid
AU - Al-Sinawi, Shadia
AU - Al-Balushi, Mohammed S.
AU - Koh, Crystal Y.
AU - Al-Busaidi, Juma Z.
AU - Idris, Mohamed A.
AU - Al-Jabri, Ali A.
N2 - 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.
AB - 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.