Location: Foodborne Toxin Detection and Prevention Research
Title: Abrin toxin paradoxically increases protein synthesis in stimulated CD4+ T-Cells while decreasing protein synthesis in kidney cellsAuthor
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Hernlem, Bradley |
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Rasooly, Reuven |
Submitted to: Current Issues in Molecular Biology
Publication Type: Peer Reviewed Journal Publication Acceptance Date: 12/9/2024 Publication Date: 12/11/2024 Citation: Hernlem, B.J., Rasooly, R. 2024. Abrin toxin paradoxically increases protein synthesis in stimulated CD4+ T-Cells while decreasing protein synthesis in kidney cells. Current Issues in Molecular Biology. 46(12): 13970–13978. https://doi.org/10.3390/cimb46120835. DOI: https://doi.org/10.3390/cimb46120835 Interpretive Summary: Abrin, a toxin of the rosary pea plant, can cause the body’s immune system to attack itself. Such so-called autoimmune disease can also be caused by superantigen toxins made by some bacteria. Abrin is best known for its ability to stop the cells in the body from building proteins. Superantigens activate immune cells to multiply and produce molecules involved in immune response, too much of which are harmful. In this study, the effect of abrin was studied on kidney and immune cells. Kidney cells made less protein in response to abrin. Milk was found to reduce this effect. On the other hand, the activation of immune cells by superantigen was made stronger when abrin was present. These findings are helpful to understand toxin caused autoimmune disease in people. Technical Abstract: Abrin, a toxin of the rosary pea plant (Abras precatorius), has been implicated as causing an autoimmune demyelinating disease in humans but the exact mechanisms responsible for the induction of these demyelinating conditions are still unknown. Certain superantigen microbial toxins such as Staphylococcus enterotoxin type A, type D, type E or streptococcal pyrogenic exotoxin type C also lead to various diseases including autoimmune disorders of the nervous system. Superantigens trigger immune response against self-antigens. Here, the effect of abrin toxin on the immune reaction was studied in human CD4+ T-cell lines. Abrin toxin inhibits protein synthesis as demonstrated with Vero (kidney) cells and milk competitively reduces this effect. However, here it is shown for the first time that abrin induces signal activation in stimulated T-cells, leading to excessive NFAT pathway activation and cytokine secretion in a dose dependent manner. This report shows that abrin amplifies antigen induced secretion of interleukin-2 (IL-2) by SEA activated CCRF-CEM cells and Jurkat cells activated by SED, SEE or SPE-C. Dose dependent secretion of interferon-' (INF') was also observed in SEE activated Jurkat cells. Abrin’s ability to boost production and release of cytokines by CD4+ T-cells may be a mechanism by which abrin toxin triggers autoimmune disease in people exposed to low doses of the toxin. |