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VacA inhibits T cell activation and proliferation via two mechanisms. First,
the anion-selective channel activity of this toxin depolarizes the plasma
membrane and prevents the opening of the CRAC calcium channel. At low levels
of cytosolic calcium, calcineurin does not dephosphorylate NFAT, thus preventing
its translocation into the nucleus and the activation of the expression of
IL-2 and IL-2 receptor, which is necessary for proliferation. Second, low
doses of VacA or its COOH-terminal domain p58 inhibit T cell activation by
inducing a cascade of phosphorylation events involving Vav and MKK3/6. This
causes an increase in the active form of p38, but not of Erk, which may
induce anergy. In addition, Vav induces actin rearrangement through the small
GTPase Rac, which leads to inhibition of T cell proliferation.
See the related article by Boncristiano et al.
(pp. 1887-1897)
and the Commentary by Montecucco and de Bernard
(pp. 1767-1771).
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