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The role of B-cells in the pathophysiology of lupus nephritis (LN) is suspected since decades. Amazingly, a report from 1977, aimed at describing the pathological characteristics of human LN described ‘proliferation of plasma cells (PCs) and plasmacytoid mononuclear cells’ in the spleen and the bone marrow (BM), but not in the kidneys.1 In murine lupus, Dixon's group discovered that polyclonal B-cell activation was the first detectable immunological abnormality in all strains, which could be observed as early as after 2 weeks of age.2 Somewhat later, the same group postulated that murine lupus can be divided into two main types: type 1 murine systemic lupus erythematosus (SLE) (NZB/W and BXSB strains), characterised by primary B-cell hyperresponsiveness to B-cell growth and differentiation factors and type 2 murine SLE (MRL/lpr strain), characterised by T-helper cell hyperactivity and overproduction of B-cell growth factors by proliferating T cells.3 A step forward was the discovery by Talal's group that besides polyclonal B-cell activation, a more restricted autoantibody response occurred with time, as suggested by a preferential use of some VH genes by certain MRL/lpr mice,4 thereby leading to further work demonstrating the presence of somatic mutations, affinity maturation and isotype switching as critical mechanisms of pathogenic anti-DNA antibody production in murine and human lupus.
Plasmablasts and PCs
The production of autoantibodies depends on the capacity of activated and proliferating autoimmune B-cells to become autoantibody-secreting cells (ASCs). During this process, B-cells progressively lose their proliferating ability but increase their autoantibody production. Two types of ASCs have been described: plasmablasts (PBs) and PCs, the former being the precursor of the latter.5 PBs are CD19+ CD20 …
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