Miller et al. reveal that B cells are able to repair damage to their plasma membranes, but this process may inhibit their ability to mount an immune response.
Eukaryotic cells quickly repair plasma membrane wounds through a pathway that culminates in the endocytosis of the damaged membrane through caveolae internalization. B lymphocytes may be particularly susceptible to damage as they squeeze their way through various tissues, sometimes directly encountering the pore-forming toxins secreted by certain pathogens. But B cells don’t express caveolins, the main components of caveolae, making it unclear whether they can repair any damage they sustain.
Miller et al. found that B cells initially respond to plasma membrane wounds like other cell types do; calcium influx induced lysosome exocytosis and the release of an enzyme, acid sphingomyelinase, that generates ceramide-rich lipid rafts at the wound site. In most cell types, caveolins are then recruited to these rafts in order to induce their endocytosis. In B cells, however, raft endocytosis and wound repair occurred independently of caveolins.
Lipid rafts are also critical for the activation and endocytosis of B cell receptors (BCRs). Miller et al. found that plasma membrane wounding inhibited BCR signaling and internalization, probably because lipid raft components were diverted towards the process of wound repair. Senior author Wenxia Song says that the competition for lipid rafts might therefore delay the activation of damaged B cells. She now wants to investigate how B cell plasma membrane wounding and delayed activation affect immune responses.