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Aims: Inflammation can trigger hyperglycemia in people with type 1 diabetes (T1D). Vaccines purposefully intend to cause an acute immunogenic response, and booster vaccines may cause even more potent immunologic responses. However, the effects of vaccines on glycemic control and insulin requirements in the days immediately post-vaccination remains poorly understood. The aim of this study was to examine the changes in glycemic control and insulin usage immediately preceding and following a COVID-19 booster vaccine among adults with T1D., Methods: In this prospective cohort study of adults with T1D, participants wore blinded Dexcom G6 Pro continuous glucose monitors for 10 days. After a baseline period, participants received a COVID-19 booster vaccine, and subsequent changes in glycemic indices were evaluated., Results: Among the 21 enrolled participants, 38% received a Moderna and 62% Pfizer-BioNTech booster. Compared to baseline (162.9 ± 44.1 mg/dL), mean glucose was significantly increased at Day 2 (172.8 ± 47.0 mg/dL; p = 0.04) and Day 3 (173.1 ± 45.0 mg/dL; p = 0.02) post-vaccination. Insulin resistance was also increased on Day 2 (p = 0.03). There were no differences in outcome metrics between booster vaccine manufacturers., Conclusions: These results suggest that adults with type 1 diabetes may experience transient mild glycemic elevations after receiving a COVID-19 booster vaccination. Studies examining the effects of other vaccines are warranted., Competing Interests: Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: M.Z. reports consulting for EMD Serono. A.P.D. received research funding from DexCom, Inc. Other authors have nothing to disclose., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Macrophages display two activation states that are considered mutually exclusive: classical macrophage activation (CMA), inducible by IFNG, and alternative macrophage activation (AMA), inducible by IL4 and IL13. CMA is prominent in allograft rejection and AMA is associated with tissue remodeling after injury. We studied expression of AMA markers in mouse kidney allografts and in kidneys with acute tubular necrosis (ATN). In rejecting allografts, unlike interferon gamma (IFNG) effects and T-cell infiltration that developed rapidly and plateaued by day 7, AMA transcripts (Arg1, Mrc1, Mmp12 and Ear1) rose progressively as tubulitis and parenchymal deterioration developed at days 21 and 42, despite persistent IFNG effects. AMA in allografts was associated with transcripts for AMA inducers IL4, IL13 and inhibin A, but also occurred when hosts lacked IL4/IL13 receptors, suggesting a role for inhibin A. Kidneys with ATN injured by ischemia/reperfusion also had increased expression of AMA markers and inhibin A. Thus kidneys undergoing T-cell-mediated rejection progressively acquire macrophages with alternative activation phenotype despite strong local IFNG effects, independent of IL4 and IL13. Although the mechanisms and causal relationships remain to be determined, high AMA transcript levels in rejecting allografts are strongly associated with and may be a consequence of parenchymal deterioration similar to ATN.