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Juan M Inclan-Rico, De’Broski R Herbert, T Regulatory Cells Influence Decisions between Concomitant Immunity versus Sterile Cure, The Journal of Immunology, Volume 207, Issue 1, July 2021, Pages 3–4, https://doi.org/10.4049/jimmunol.2100338
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Host-protective immunity is dependent upon the generation of inflammatory responses that mediate pathogen clearance, but if left unchecked, it can result in excessive tissue pathology. It is now established that distinct T lymphocyte populations serve inflammatory versus suppressive roles, but these functions are often subverted by pathogens that have evolved countermeasures allowing their chronic persistence. In contrast to acute infections that evoke sterilizing immunity, in which infectious organisms are no longer detectable, some chronic infections can result in the persistence of low amounts of infectious particles, as observed in patients infected with the parasites Trypanosoma cruzi or Toxoplasma gondii (1, 2). The low-level persistence of pathogens raises the long-standing debate as to whether immunological memory that protects against reinfection requires T cells to be constantly exposed to Ag or live pathogens. During chronic infections, the long-term persistence of reduced pathogenic loads after a primary infection, despite being protected against secondary exposures, is defined as “concomitant immunity” (3). A similar phenomenon has been described in helminth infections with Schistosoma mansoni and filarial nematodes, in which infection with adult worms provides effective defense against larval stages (4, 5), suggesting that parasites may represent invaluable experimental systems to study these host-pathogen interactions. Whether concomitant immunity emanated from host manipulation by parasites or is a coevolutionary adaptation of host immune responses that strikes a balance between pathogen clearance and tissue immunopathology has remained an important issue since the 1970s.