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Sweat is an exacerbation factor in atopic dermatitis (AD) in all age groups. A body core temperature elevation with sweating triggers cholinergic urticaria (CholU). We recently reported that AD symptoms are improved by tannic acid-containing spray, which suppresses the basophil histamine release induced by semi-purified sweat antigen in vitro, and by showering, which removes antigens in sweat from the skin surface. Sweat contains small amount of proteins including proteases, protease inhibitors, and anti-microbial peptides. We finally identified MGL_1304 secreted by Malassezia (M.) globosa as a major histamine - releasing antigen in human sweat. MGL_1304 is a 17-kDa protein in sweat that elicits almost the highest histamine - release activity from basophils of patients with AD and CholU among antigens derived from Malassezia species. Moreover, serum levels of anti-MGL_1304 IgE were significantly higher in patients with AD and CholU than in normal controls. The recombinant protein produced by Pichia pastoris possessed comparable allergenicity to native MGL_1304. We found a monoclonal IgE antibody against MGL_1304 which did not elicit histamine release from sensitized mast cells. Desensitization therapy using autologous sweat, or MGL_1304 purified from culture of M. globosa or its cognates might be beneficial for patients with intractable CholU due to sweat allergy.

Immune checkpoint inhibitors (ICI) have been administrated as a standard medication in many cases of malignant melanoma (MM). They may be effective even for MM in advanced stages. However, it is still challenging to reduce the burden of MM, which were or became refractory to ICI, especially those without BRAF gene mutation. Re‐administration of ICI after other modalities of treatment may be an option of treatment, but the efficacy and safety of retreatment with ICI have not been well established. We experienced four patients with advanced MM retreated with programmed cell death 1 (PD‐1) inhibitor. All cases were refractory to the first PD‐1 inhibitor, nivolumab, and then treated with dacarbazine (DTIC), followed by pembrolizumab. Two of the four cases achieved a partial response by switching to pembrolizumab as the second PD‐1 inhibitor, and the other two cases resulted in progressive disease. In all cases, no new severe adverse events developed upon PD‐1 inhibitor retreatment. Even if the first PD‐1 inhibitor proves to be ineffective, it is worth re‐administrating PD‐1 inhibitor following a bridging therapy with DTIC.

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