Date
December 17 (Thu) at 10:00 - 11:00, 2020 (JST)
Speaker
  • Akane Hara (Ph.D. Student, Graduate School of Systems Life Sciences, Kyushu University)
Venue
  • via Zoom
Language
English

The pathogen with proteins similar to host’s proteins is likely to cause autoimmunity, which is called “molecular mimicry”. To understand the mechanism of autoimmunity development caused by pathogen infection, we considered the following scenario: the infection activates the immune system, which results in clearance of pathogens, and the enhanced immune responses to the host’s body may remain and attack the host’s cells after the pathogen clearance. We developed a mathematical model describing the dynamics of T helper (Th) cells, viruses, self-antigens, and memory T cells and identified the conditions necessary to realize the scenario. We considered the cross-immunity of three different modes of action: [1] virus elimination by Th cells reactive to the self-antigen, [2] activation of Th cells reactive to viruses by self-antigens and Th cells reactive to self-antigens by viruses, and [3] enhancement of immune responses to self-antigens by Th cells reactive to viruses after the infection. The cross-immunity of type [3] was found to be most important for autoimmunity development. In contrast, [1] and [2] suppressed autoimmunity by effectively decreasing the viral abundance.

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