For those who aren’t already aware of it, we direct you to the Th17 review series showcased in the February issue of CEI that features a superb authorship addressing a range of questions relating to this fast-developing field, including Robert Lechler, Giovanni Lombardi, Steve Anderton, Graham Lord and Leonie Taams (who also put in sterling work coordinating and guest-editing the reviews).

 

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An intriguing aspect of IgG antibodies is that they can have two completely opposite effects. During infection, or as part of autoimmune disease pathology, they induce proinflammatory responses and recruit innate immune effector cells. On the other hand, intravenous infusion of high doses of pooled IgG molecules during IVIG therapy represents an efficient anti-inflammatory treatment for many autoimmune diseases. Whereas our understanding of the former mechanism is quite advanced, we are only at the very beginning to comprehend how the latter comes about. Here Nimmerjahn et al. summarise our current knowledge and focus upon the two major explanatory models: IVIG-mediated competition for IgG-triggered effector functions or IVIG-mediated adjustment of cellular activation thresholds.