Host-pathogen interactions during acute or chronic infections reset the levels and activation state of the immune system and differences in immune response have been observed in immune-related disorders including infection, inflammation, autoimmunity, cancer and immune response to immunotherapy. Interestingly, the Epstein Barr virus (EBV) infection established causative factor for multiple sclerosis, seems to be protective in type 1 diabetes based on the positive response to the immunomodulating therapy with Teplizumab in EBV seropositive type 1 diabetes individuals. This phenomenon may be explained by the partial exhaustion of CD8+T cells and positive response of the regulatory T cells (Treg). Taking together, the effect of EBV on the host predisposition to the autoimmunity has to be considered in the immune context of the host and can not to be excluded that the latency of EBV may have a protective effects.

Is Epstein Barr virus latency protective against type 1 diabetes?

Zoledziewska M.
Conceptualization
2024

Abstract

Host-pathogen interactions during acute or chronic infections reset the levels and activation state of the immune system and differences in immune response have been observed in immune-related disorders including infection, inflammation, autoimmunity, cancer and immune response to immunotherapy. Interestingly, the Epstein Barr virus (EBV) infection established causative factor for multiple sclerosis, seems to be protective in type 1 diabetes based on the positive response to the immunomodulating therapy with Teplizumab in EBV seropositive type 1 diabetes individuals. This phenomenon may be explained by the partial exhaustion of CD8+T cells and positive response of the regulatory T cells (Treg). Taking together, the effect of EBV on the host predisposition to the autoimmunity has to be considered in the immune context of the host and can not to be excluded that the latency of EBV may have a protective effects.
2024
Istituto di Ricerca Genetica e Biomedica - IRGB
EBV, type 1 diabetes, multiple sclerosis, CD8+ T cells, regulatory T cells, Teplizumab
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.14243/467365
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