Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

B lymphocytes are key players in host defence, but also autoimmune diseases. Their survival depends upon tonic signals transduced by surface immunoglobulin (BCR) and the process leading to antibody secretion is initiated by interaction of BCR with a cognate antigen. CD22 limits signalling of the BCR to strike a balance between tonic signalling, reactivity to pathogens and prevention of autoimmunity. In this issue, Gasparrini et al (2016) combined super‐resolution imaging approaches with single‐particle tracking and simulations to show how CD22 controls the signalling state of the BCR. They demonstrated that small CD22 nanoclusters run rings around the BCR in confined steady state to maintain low tonic signals, but releasing BCR from these corrals allows BCR cluster growth, which overcomes the harrying inhibition from highly mobile CD22.

Original publication

DOI

10.15252/embj.201593745

Type

Report

Publisher

Springer Science and Business Media LLC

Publication Date

02/2016

Volume

35

Pages

237 - 238