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Adalimumab as a successful alternative for the treatment of infliximab‐induced sarcoidosis

infection were excluded by thorough examinations. Transbronchial lung biopsy demonstrated non-caseating granuloma formation and inflammatory cell infiltration (Fig. 1b). Melan-A, S-100 and HMB-45 cells were not found, thus excluding melanoma cells. Infiltrating lymphocytes were CD4 and CD8 cells, with the former outnumbering the latter (Fig. 1c,d). Ophthalmologic examination revealed corneal posterior deposit and full iris adhesion. No sarcoid-related lesion was found in the skin, heart, nerves or kidney; the lung and eye lesions were diagnosed as sarcoid-like reactions. Concomitantly, he developed widespread vitiligo lesions, starting on his head, scrotum and trunk (Fig. 1e). Skin biopsy from a vitiligo lesion on the back revealed lymphocytic infiltration at the dermoepidermal junction (Fig. 1f). CD8 T cells infiltrated the dermoepidermal junction, whereas CD4 cells were scattered in the dermis (Fig. 1g,h). Oral prednisolone (20 mg/day) was initiated; the exertional dyspnea and ocular symptoms improved. However, following prednisolone dose reduction, the ocular symptoms relapsed, and LN and lung lesions, indicating melanoma metastases, increased. Although nivolumab was re-administrated, new metastatic lesions continued to develop; 1.5 years after the first visit, the patient died. Anti-PD-1 antibody promotes activation of CD8 T cells and secretion of cytokines including interferon (IFN)-c and IL-2. This is speculated to be the underlying mechanism of the therapeutic effect and adverse reaction associated with this antibody. In sarcoidosis, T-helper 1 cells generally produce IFN-c and IL-2, inducing macrophage activation and local inflammation. Meanwhile, melanogenesis-related peptide-specific CD8 T cells are involved in the pathogenesis of vitiligo. Our case indicates that effector T cells may differ depending on the irAE type, CD4 T cells in sarcoidosis and CD8 T cells in vitiligo. Simultaneous occurrence of these two irAE suggests that antiPD-1 antibody treatment is capable of orchestrating complex immune reactions, triggering enhancement of multiple effector T-cell types.