IFN-γ-induced MHCII+ inflammatory monocytes play a role for down-regulating CD8 T cell responses in acute LCMV infection

• Published in: The Journal of immunology (1950) 2017-05, Vol.198 (1_Supplement), p.78-78.39
• Main Authors: Shin, Kwang-Soo, Park, Young-Jun, Koh, Choong-Hyun, Bae, Eun-Ah, Kim, Il-Kyu, Song, Boyeong, Seo, Hyungseok, Jeon, Insu, Kang, Chang-Yuil
• Format: Article
• Language: English
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.198.Supp.78.39

During viral infection, monocytes play a protective role for clearance of pathogens. However, little is known about the role of recruited monocytes after effector phase, especially as regard to their effects to T cells. Here, we have investigated the phenotypes, the origin and inducing factor, and the effects to CD8 T cells of inflammatory monocytes in virus-infected mice. During Lymphocytic choriomeningitis virus (LCMV)-Arm infection, CCR2+ inflammatory monocytes were accumulated in lymphoid organs and reached their peak at day 8 post infections. Inflammatory monocytes of infected mice expressed high levels of MHCII and low levels of CD11c, which overlap with phenotypes of DC and those of macrophage, respectively. We found that IFN-gamma (IFN-γ) is a factor that differentiates MHCII+ monocytes from BM progenitor cells. Among the BM progenitor cells, common monocyte progenitors (cMoPs) were rapidly converted to MHCII+ inflammatory monocytes in response to GM-CSF and IFN-γ in vitro. In addition, cMoPs that were adoptively transferred to infected recipients were differentiated to MHCII+ inflammatory monocytes. We also found that MHCII+ monocytes-primed CD8 T cells could not produce inflammatory cytokine and granzymeB efficiently, implicating their lowered effector functions, despite their comparable proliferative capacity to conventional DC-primed CD8 T cells. Overall, our data suggest that IFN-γ-induced MHCII+ inflammatory monocytes during acute LCMV infection would play a role in down-regulating CD8 T cell responses.