Type 1 diabetes mellitus (T1DM) is characterized by irreversible islet β cell destruction. During the progression of this disease, some patients with T1DM experience a phase of remission known as honeymoon or partial remission (PR) that is mainly characterized by satisfactory glycemic control and the transient recovery of islet β cell function. This special phase is a good model for studying the mechanism of β cell protection, might serve as a proper intervention period for immunotherapy, and may be related to disease prognosis. This special stage is highly valuable for studies aiming to identify possible targets that may be used to cure T1DM. An in-depth understanding of the diagnosis, epidemiology, and possible mechanisms of the PR phase is highly needed. In general, patients enter the PR phase approximately 3 months after starting insulin therapy, and this phase could be sustained for 6 to 9 months. Current research increasingly focuses on the metabolic and immunological aspects to constantly update our understanding of this phase. This review concentrates on the PR phase of T1DM to provide a comprehensive outlook of its epidemiology, diagnostic criteria, and underlying immune metabolic mechanisms. KEYWORDSimmuno-metabolic mechanism, remission phase, the honeymoon period, type 1 diabetes

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Tumor-associated macrophages (TAMs) are one of the most abundant immunosuppressive cells in the tumor microenvironment and possess crucial functions in facilitating tumor progression. Emerging evidence indicates that altered metabolic properties in cancer cells support the tumorigenic functions of TAMs.However, the mechanisms and mediators the underly the cross-talk between cancer cells and TAMs remain largely unknown. In the present study, we revealed that high solute carrier family 3 member 2 (SLC3A2) expression in lung cancer patients was associated with TAMs and poor prognosis. Knockdown of SLC3A2 in lung adenocarcinoma cells impaired M2 polarization of macrophages in a coculture system. Using metabolome analysis, we identified that SLC3A2 knockdown altered the metabolism of lung cancer cells and changed multiple metabolites, including arachidonic acid, in the tumor microenvironment. More importantly, we showed that arachidonic acid was responsible for SLC3A2-mediated macrophage polarization in the tumor microenvironment to differentiate into M2 type both in vitro and in vivo. Our data illustrate previously undescribed mechanisms responsible for TAM polarization and suggest that SLC3A2 acts as a metabolic switch on lung adenocarcinoma cells to induce macrophage phenotypic reprogramming through arachidonic acid.