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Neurology. 2018 Dec 11;91(24):e2233-e2237. doi: 10.1212/WNL.0000000000006648. Epub 2018 Nov 7.

Vitiligo after alemtuzumab treatment: Secondary autoimmunity is not all about B cells.

Author information

1
From the Clinic of Neurology with Institute of Translational Neurology (T.R., S.P., A.S.-M., C.C.G., M.L., H.W., S.G.M., L.K.) and Department of Dermatology (D.M., J.E.), University of Münster; and Departments of Dermatology, Venereology, and Allergology (W.S.) and Neurology (R.P., C.K.), University School of Medicine Essen-Duisburg, Essen, Germany. tobias.ruck@ukmuenster.de.
2
From the Clinic of Neurology with Institute of Translational Neurology (T.R., S.P., A.S.-M., C.C.G., M.L., H.W., S.G.M., L.K.) and Department of Dermatology (D.M., J.E.), University of Münster; and Departments of Dermatology, Venereology, and Allergology (W.S.) and Neurology (R.P., C.K.), University School of Medicine Essen-Duisburg, Essen, Germany.

Abstract

OBJECTIVE:

To report 3 patients with relapsing-remitting multiple sclerosis (RRMS) showing vitiligo after treatment with alemtuzumab.

METHODS:

Retrospective case series including flow cytometric analyses and T-cell receptor (TCR) sequencing of peripheral blood mononuclear cells.

RESULTS:

We describe 3 cases of alemtuzumab-treated patients with RRMS developing vitiligo 52, 18, and 14 months after alemtuzumab initiation. Histopathology shows loss of epidermal pigmentation with absence of melanocytes and interface dermatitis with CD8+ T-cell infiltration. Also compatible with pathophysiologic concepts of vitiligo, peripheral blood mononuclear cells of one patient showed high proportions of CD8+ T cells with an activated (human leukocyte antigen-DR+), memory (CD45RO+), and type 1 cytokine (interferon-γ + tumor necrosis factor-α) phenotype at vitiligo onset compared to a control cohort of alemtuzumab-treated patients with RRMS (n = 30). Of note, analysis of CD8 TCR repertoire in this patient revealed a highly increased clonality and reduced repertoire diversity compared to healthy controls and treatment-naive patients with RRMS. We observed a predominance of single clones at baseline in this patient and alemtuzumab treatment did not substantially affect the proportions of most abundant clones over time.

CONCLUSION:

The 3 cases represent a detailed description of vitiligo as a T-cell-mediated secondary autoimmune disease following alemtuzumab treatment. The prevailing concept of unleashed B-cell responses might therefore not cover all facets of alemtuzumab-related secondary autoimmunity. Mechanistic studies, especially on TCR repertoire, might help clarify the underlying mechanisms.

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