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Chronic Parasitic Infection Maintains High Frequencies of Short-Lived Ly6CCD4 Effector T Cells That Are Required for Protection against Re-infection
Naturally acquired resistance to reinfection by numerous infectious pathogens including Leishmania, Plasmodium, Mycobacterium, and parasitic worms, typically coincides with an ongoing primary infection. This natural resistance to reinfection, termed concomitant immunity, is often referred to as a memory response and provides the rationale for the vaccine effort against these infectious pathogens. However, immune memory is mediated by populations of long-lived cells that do not require an ongoing primary infection to mediate protection. The requirement for chronic infection to maintain concomitant immunity suggests that the critical cells that mediate this immunity are not memory cells. In the present study we define short-lived effector T cells that pre-exist secondary challenge, not memory cells, as the critical cells that mediate concomitant immunity. These observations provide direct evidence on a cellular level that conventional vaccination strategies against chronic infectious diseases, whose development is predicated upon the belief that concomitant immunity can be mediated by long-lived memory cells, are unlikely to succeed.
Vyšlo v časopise: Chronic Parasitic Infection Maintains High Frequencies of Short-Lived Ly6CCD4 Effector T Cells That Are Required for Protection against Re-infection. PLoS Pathog 10(12): e32767. doi:10.1371/journal.ppat.1004538
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1004538Souhrn
Naturally acquired resistance to reinfection by numerous infectious pathogens including Leishmania, Plasmodium, Mycobacterium, and parasitic worms, typically coincides with an ongoing primary infection. This natural resistance to reinfection, termed concomitant immunity, is often referred to as a memory response and provides the rationale for the vaccine effort against these infectious pathogens. However, immune memory is mediated by populations of long-lived cells that do not require an ongoing primary infection to mediate protection. The requirement for chronic infection to maintain concomitant immunity suggests that the critical cells that mediate this immunity are not memory cells. In the present study we define short-lived effector T cells that pre-exist secondary challenge, not memory cells, as the critical cells that mediate concomitant immunity. These observations provide direct evidence on a cellular level that conventional vaccination strategies against chronic infectious diseases, whose development is predicated upon the belief that concomitant immunity can be mediated by long-lived memory cells, are unlikely to succeed.
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Štítky
Hygiena a epidemiológia Infekčné lekárstvo Laboratórium
Článek Selective Susceptibility of Human Skin Antigen Presenting Cells to Productive Dengue Virus InfectionČlánek P47 Mice Are Compromised in Expansion and Activation of CD8 T Cells and Susceptible to InfectionČlánek Molecular Evolution of Broadly Neutralizing Llama Antibodies to the CD4-Binding Site of HIV-1
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