Inflammatory monocytes hinder antiviral B cell responses

Abstract

LCMV evades B cell responses by recruiting inflammatory monocytes to draining lymph nodes. See related Research Articles by Fallet et al. and Moseman et al. and a Focus by Laidlaw et al.

Transcriptional correlates of malaria in RTS,S/AS01-vaccinated African children: a matched case–control study

“…Note that the ML ratio in these studies was based on lymphocyte count and monocyte count from a differential blood count performed using a Coulter Counter, and thus cannot inform on the gene expression profiles of the circulating monocytes, or on composition of circulating monocyte subsets. Based on previous evidence in various mouse models of viral infection that inflammatory monocytes inhibit T-cell proliferation ( Norris et al, 2013 ; Mitchell et al, 2012 ), T-cell activation ( Mitchell et al, 2012 ), and B-cell responses ( Sammicheli et al, 2016 ), Warimwe et al proposed that inflammatory monocytes may inhibit RTS,S-induced protective adaptive responses. Our gene-level correlates analyses suggest an alternative hypothesis, however.…”

Communicating Science Effectively: When an Optimised Video Communication Enhances Comprehension, Pleasantness, and People’s Interest in Knowing More About Scientific Findings

“…One half of them watched an existing non-optimised video communication on the discovery of a biological mechanism that some viruses would exploit to prolong their persistence within the host. Such video was originally and officially intended to disseminate the research findings by Sammicheli et al (2016). The other half watched a new (ad-hoc created) optimised video, with the same scientific content.…”

Immunometabolism of Myeloid-Derived Suppressor Cells: Implications for Mycobacterium tuberculosis Infection and Insights from Tumor Biology

“…Other signaling molecules such as HIF-1α and nuclear respiratory factor (NRF) are critical in conditions of hypoxia and pathways that modulate MDSC differentiation, allowing them to take a dual M1/M2 phenotype and mTOR-induced glycolytic activities [ 32 , 134 , 156 ] and contribute to immune cell reprogramming. In addition, Nrf2 promotes the expression of NAD(P)H-quinone oxidoreductase 1 (NQO1), the enzyme responsible for the reduction and detoxification of reactive quinones, and the enzyme responsible for the cleavage of heme into biliverdin, heme oxygenase of expression-1 (HMOX1) [ 157 ]. Interestingly, HMOX1 functions in part as an antioxidant but has also been shown to be anti-inflammatory, reducing IL-12 p40, IL-16, and TNF-α levels in dendritic cells and in allergic airways [ 158 ].…”

“…In a study of murine infected with the lymphocytic choriomeningitis virus (LCMV), virus-specific B cells interacting with myeloid cells were inhibited and eventually killed by a population of CD11b + Ly6C hi inflammatory monocytes [ 157 ]. These myeloid cells were recruited through a type-1 interferon (IFN-1) and CCR2-dependent mechanism, and they suppressed antiviral B-cell response by virtue of their ability to produce NO [ 157 ].…”

“…In a study of murine infected with the lymphocytic choriomeningitis virus (LCMV), virus-specific B cells interacting with myeloid cells were inhibited and eventually killed by a population of CD11b + Ly6C hi inflammatory monocytes [ 157 ]. These myeloid cells were recruited through a type-1 interferon (IFN-1) and CCR2-dependent mechanism, and they suppressed antiviral B-cell response by virtue of their ability to produce NO [ 157 ]. Similarly, Fooksman et al also showed that macrophages and Gr-1-negative monocytes such as the CX3CR1 + subset were able to dampen the numbers of antibody-secreting cells (ASC) and titers possibly through secretion of IL-10.…”