Helminth-induced immune regulation: implications for immune responses to tuberculosis.

Tuberculosis (TB) caused by the bacteriaMycobacterium tuberculosis (Mtb) remains a global cause of considerable morbidity and mortality [1]. One of the biggest current challenges of TB control is our incomplete understanding of what constitutes protective immunity in TB-endemic areas of the world. Although close to 2,200 million people maintain the infection in a state of latency and act as a reservoir of infection, the risk factors for reactivation to active dis-ease and subsequent transmission in these populations are poorly understood. These areas also report some of the lowest rates of efficacy of the Bacillus Calmette–Guérin (BCG) vaccine [2]. Helminth infections (soil transmitted and vector-borne) exhibit broad geographic overlap with areas of TB endemicity [3]. These complex eukaryotes have the ability to establish chronic, often asymptomatic infections and have evolved highly effective methods for subverting the immune system for their survival. Their immunomodulatory effects (as we discuss below) have been shown to extend to nonparasitic infections and vaccine responses [4, 5]. Our knowledge of how helminth-coinfection-induced immune regulation can affect TB-specific immunity and disease in an endemic area comes from three broad areas of study, with specific animal models providing supplemental evidence for particular immunologic phenomena at various stages of

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