T cell response and persistence of the microsporidia

Authors

  • Kaya Ghosh,

    1. Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY, USA
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  • Louis M. Weiss

    Corresponding author
    1. Division of Tropical Medicine and Parasitology, Department of Pathology, Albert Einstein College of Medicine, Bronx, NY, USA
    2. Division of Infectious Diseases, Department of Medicine, Albert Einstein College of Medicine, Bronx, NY, USA
    • Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY, USA
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Correspondence: Louis M. Weiss, Division of Infectious Diseases, Department of Medicine, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Room 504 Forchheimer, Bronx, NY 10461, USA. Tel.: +1 718 4302142; fax: +1 718 4308543; e-mail: louis.weiss@einstein.yu.edu

Abstract

The microsporidia are a diverse phylum of obligate intracellular parasites related to the fungi that cause significant and sometimes life-threatening disease in immune-compromised hosts, such as AIDS and organ transplant patients. More recently, their role in causing pathology in immune-competent populations has also been appreciated. Interestingly, in several instances, the microsporidia have been shown to persist in their hosts long term, causing at opposite ends of the spectrum either an intractable chronic diarrhea and wasting in patients with advanced-stage AIDS or asymptomatic shedding of spores in healthy populations. Much remains to be studied regarding the immune response to these pathogens, but it seems clear that CD8+ T cells are essential in clearing infection. However, in the infection models examined thus far, the role for CD4+ T cells is unclear at best. Here, we discuss the possible reasons and ramifications of what may be a weak primary CD4+ T cell response against Encephalitozoon cuniculi. Given the central role of the CD4+ T cell in other models of adaptive immunity, a better appreciation of its role in responding to microsporidia may provide insight into the survival strategies of these pathogens, which allow them to persist in hosts of varied immune status.

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