Cutting Edge: Hierarchy of Maturity of Murine Memory B Cell Subsets

Abstract

The paucity of murine memory B cell markers has been a significant impediment to the study of memory. The most commonly used marker is IgG, which is neither sensitive nor specific, because activated nonmemory cells can be IgG+, and memory cells can be IgM+. In this article, we show that, together, PD-L2 (CD273), CD80, and CD73 define at least five phenotypic subsets of murine memory B cells. These subsets are generated from naive cells bearing a single BCR in response to a single T-dependent Ag. This diversity is independent of class switch, because IgG1- and IgM-bearing memory cells are found within each compartment. Memory subsets defined by PD-L2, CD80, and CD73 are biologically distinct from one another, because they differ in ontogeny and selection. Together, these distinctions suggest that there is a spectrum of memory B cells and progressive acquisition from more naive-like to more memory-like properties.

Memory B cells in the lung participate in protective humoral immune responses to pulmonary influenza virus reinfection

“…This process resembles the slower accumulation of plasma cells in the lungs after influenza virus infection (11) and may reflect a requirement for structural alteration and/ or niche formation in the infected lungs for B-cell localization. Although definitive markers of murine memory B cells remain to be identified (12,13), CD73, CD80, and CD273 (PD-L2) are expressed at higher levels on splenic memory than on naïve B cells (14,15). It is also postulated that the proportions of CD80 (6).…”

Mouse CMV infection delays antibody class switch upon an unrelated virus challenge

“…We recently showed that MCMV induces poor CD8 T-cell response to challenges with emerging viral infections and that this poor response correlates to the frequency of the (Dogan et al, 2009;Pape et al, 2011;Tomayko et al, 2010). IgM memory B-cells persist long after the clearance of an infection, whereas the conventional memory cells are described as the frontline responders to infections (Good-Jacobson and Tarlinton, 2012).…”

Aberrant B-cell homeostasis in chronic GVHD

“…55 Similar murine "memory" B-cell subsets have also been identified, making it possible to examine the pathogenic role of these BCR-activated B-cell subsets in murine models. 56,57 Recent studies have revealed significant increases in B-cell activation in cGVHD. Compared with B cells in patients without cGVHD, purified peripheral cGVHD B cells were found to be enlarged in size and to contain more total protein per cell, indicating heightened metabolic activity in vivo.…”