AsianScientist (Dec. 24, 2014) – Plasmablasts, the immature version of antibody secreting cells known as plasma cells, have been shown to be the source of the anti-inflammatory cytokine IL-10 in mouse models of autoimmune disease. The study documenting these findings has been published in Immunity.
The role of the immune system in the body is to differentiate between “self” and “non-self”, only attacking things that are recognized as “non-self”. However, once the immune system has broken down, it attacks the self’s normal cells and tissues, causing autoimmune disorders such as multiple sclerosis (MS), rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE).
Although the mechanism for development of MS has not been clarified, it is thought to be caused by the destruction of the myelin sheath by immune cells. In recent years, it has been reported that B cells producing IL-10—referred to as regulatory B cells—suppress experimental autoimmune encephalomyelitis (EAE) in MS mouse models. To date, how regulatory B cells are classified and the mechanism through which they suppress encephalomyelitis has not be clarified.
By using IL-10 reporter mice, a team of researchers from Osaka University found that plasmablasts in the draining lymph nodes (dLNs), but not splenic B lineage cells, were the main source of IL-10 during EAE. Mice lacking plasmablasts by genetic ablation of the transcription factors Blimp1 or IRF4 in B lineage cells developed an exacerbated EAE.
The research team also showed that IRF4 positively regulated IL-10 production, thereby inhibiting dendritic cell function to generate pathogenic T cells. These findings could lead to the development of new treatments for MS, provided that the differentiation of IL-10-producing plasmablasts can be controlled.
The article can be found at: Matsumoto et al. (2014) Interleukin-10-Producing Plasmablasts Exert Regulatory Function in Autoimmune Inflammation.
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Source: Osaka University.
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