IL4 and infection: In vitro, the pro-inflammatory phenotype has been modeled by exposure to IFNγ + LPS, and termed “classically-activated” or “M1.” After tissue injury or clearance of infection, macrophages shift to a pro-healing phenotype, modeled in vitro by exposure to IL-4 and IL-13, and termed “alternatively-activated” or “M2.” While the M1/M2 dichotomy is useful shorthand, the binary division of phenotypes oversimplifies the profound plasticity of macrophages, which can simultaneously support host-defense and tissue repair (2).