graphic

Myosin II drives the clustering of MHC vesicles (green) and endocytotic vesicles (red) containing antigen (blue) in B cells.

A cellular contraction brings antigens together with the MHC molecules that will present them, say Vascotto et al. (page 1007).

Vesicles containing endocytosed antigen and those containing MHC class II molecules come together in the cell to form specialized antigen-processing lysosomes. To investigate the mechanics of this union, Vascotto and colleagues followed events in real time by live cell microscopy.

They were surprised to see that B cells contracted soon after activation with antigen. This contraction was coupled with a clustering of MHC class II toward the center of the cell, where immunofluorescence revealed that antigen vesicles also cluster.

Cell contraction relies in part on myosin II activation. Antigen stimulation of B cells led to myosin II activation. Inhibiting myosin II blocked the cell contraction, the clustering of the vesicles, and antigen presentation at the cell surface. Endocytosis of the antigen, however, remained unaffected, indicating that general cell paralysis was not to blame.

Upon B cell stimulation with antigen, MHC molecules become hooked to the contractile actomyosin network through an interaction between myosin II and the cytosolic tail of the MHC class II chaperone, called the invariant chain. In cells lacking the invariant chain, MHC class II–containing vesicles did not cluster. Antigen-containing vesicles also did not cluster in these cells, but the authors have yet to explain this failure.

Myosin II might directly transport MHC class II vesicles along actin filaments, although MHC class II vesicles were reported to travel along microtubules in other cell types. Exactly how myosin II relocates MHC class II vesicles is currently under investigation.