Cell Mediated Immunity

Cell Mediated Immunity-a (small) Victory for Hosts Everywhere
Hurray for the host! There exists a study describing a case in which the host immune response, in a rare instance, does what it is supposed to do when infected with B. anthracis. Guidi-Rontani et al detail how lethal toxin (LeTx) stimulated proliferation of peripheral T-cells, at least in vitro (21).

Aside from this study, however, the story is short and predictable. B. anthracis has evolved effective mechanisms to squelch cell mediated immunity (22, 23, 24). Both LeTx and edema factor (EF) have roles in suppressing T-cell chemotaxis. These virulence factors work by disrupting the signaling pathways from the CXC and CC chemokine receptors (22). These two toxins also disrupt MAPK in T lymphocyte cells with the goal of inhibiting NFAT and AP-1. These are critical transcription factors which lead to the expression of chemokines upton TCR cross-linking. These effects are seen at extremely low concentrations of anthrax toxins (23). This observation is important considering that their effects would be seen early during infection in vivo, the point at which communication to and from T-cells would be most important. Other studies have confirmed this result, as T-lymphocytes isolated from mice injected with low levels of LeTx and EF responded to neither CD3 nor CD28 antibodies (24).