Loss of thymic function promotes EAE relapse in anti-CD52-treated mice

Adeolu O Adegoke; Jiaxin Lin; Colin C Anderson

doi:10.1016/j.crimmu.2022.03.001

Loss of thymic function promotes EAE relapse in anti-CD52-treated mice

Curr Res Immunol. 2022 Mar 8:3:37-41. doi: 10.1016/j.crimmu.2022.03.001. eCollection 2022.

Authors

Adeolu O Adegoke^{1

2}, Jiaxin Lin^{1

2}, Colin C Anderson^{1

2

3}

Affiliations

¹ Department of Surgery, University of Alberta, Edmonton, Alberta, Canada.
² Alberta Diabetes and Transplant Institutes, University of Alberta, Edmonton, Alberta, Canada.
³ Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada.

Abstract

Anti-CD52 treatment creates a long-lasting CD4 T cell lymphopenia and reduces multiple sclerosis (MS) relapses in humans. In contrast, anti-CD52 therapy at disease onset more fully suppresses experimental autoimmune encephalomyelitis (EAE) in mice, and T cell repopulation is rapid. To test whether prolonged T cell lymphopenia promotes relapses, we thymectomized mice prior to EAE induction and anti-CD52 treatment. Thymectomy greatly reduced the number of recent thymic emigrant T cells and was associated with a prolonged reduction in CD4 T cells in peripheral blood. Two-thirds of thymectomized C57BL/6 mice had an EAE relapse post anti-CD52 treatment, while no surgery and sham surgery euthymic controls remained relapse-free. These data demonstrate that thymus function can alter the effectiveness of anti-CD52 treatment.

Keywords: Alemtuzumab; Anti-CD52; EAE; Multiple sclerosis; Recent thymic emigrants; Thymectomy.