Pathology of Diabetes-Induced Immune Dysfunction

被引:18
作者
Alexander, Michael [1 ]
Cho, Eric [1 ]
Gliozheni, Eiger [1 ]
Salem, Yusuf [1 ]
Cheung, Joshua [1 ]
Ichii, Hirohito [1 ]
机构
[1] Univ Calif Irvine, Dept Surg, Div Transplantat, Irvine, CA 92868 USA
关键词
diabetes; immune dysfunction; immune senescence; infection; medication side effects; vaccine uptake; latent autoimmune diabetes in adults; GLUTAMIC-ACID DECARBOXYLASE; HEPATITIS-B VACCINATION; MARROW STROMAL CELLS; BONE-MINERAL DENSITY; OXIDATIVE STRESS; INSULIN REQUIREMENT; ISLET AUTOIMMUNITY; TYPE-2; INFLAMMATION; LYMPHOPOIESIS;
D O I
10.3390/ijms25137105
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Diabetes is associated with numerous comorbidities, one of which is increased vulnerability to infections. This review will focus on how diabetes mellitus (DM) affects the immune system and its various components, leading to the impaired proliferation of immune cells and the induction of senescence. We will explore how the pathology of diabetes-induced immune dysfunction may have similarities to the pathways of "inflammaging", a persistent low-grade inflammation common in the elderly. Inflammaging may increase the likelihood of conditions such as rheumatoid arthritis (RA) and periodontitis at a younger age. Diabetes affects bone marrow composition and cellular senescence, and in combination with advanced age also affects lymphopoiesis by increasing myeloid differentiation and reducing lymphoid differentiation. Consequently, this leads to a reduced immune system response in both the innate and adaptive phases, resulting in higher infection rates, reduced vaccine response, and increased immune cells' senescence in diabetics. We will also explore how some diabetes drugs induce immune senescence despite their benefits on glycemic control.
引用
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页数:18
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