Parasitic Infections and Mutilation of T-Cell Function

Recently a review has been published in PLOS Neglected Tropical Diseases (http://www.plosntds.org/). This review focuses mainly on the development of the four intracellular parasite species (Plasmodium spp., Trypanosoma cruzi, Toxoplasma gondii and Leishmania spp.) in the mammalian hosts they infect, with special emphasis on T lymphocyte function. These parasites after invading the host, blight T cell function and augment their apoptosis. Such impairments lead the host unresponsive for the parasite because of the collapse of the T cell number. This weakening of T-cells aids the parasites to survive throughout the infection or become persistent. All of such process follows a particular tier system as:

1: Invading/breaching the host barriers and integument or epidermis.

2: Down-regulate T cell function and lead to their exhaustion.

3: Apoptosis of T-cells or T-cell contraction.

4: Stay persistently in the host.

These parasites can accomplish apoptosis of host T-cells by activation-induced cell death (AICD) involving death ligands and caspase-8 or activated T cell autonomous death (ACAD) involving Bcl-2 family. This course of action respectively results in the formation of the death-inducing signalling complex (DISC) or apoptosome. Several studies have shown that patients infected with Plasmodium falciparum, Trypanosoma cruzi and Leishmania donovani have elevated levels of death ligand FasL. Also some studies have proven that engulfment of apoptotic cells stimulates expansion of parasites like Trypanosoma cruzi and Leishmania major inside host macrophages.

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This work is Licensed under Creative Commons Licenses.

Reference: Vasco Rodrigues,  Anabela Cordeiro-da-Silva, Mireille Laforge, Ali Ouaissi, Khadija Akharid, Ricardo Silvestre mail, Jérôme Estaquier mail.. DOI: 10.1371/journal.pntd.0002567

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