Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2024 Jun 28;25(13):7105.
doi: 10.3390/ijms25137105.

Pathology of Diabetes-Induced Immune Dysfunction

Affiliations
Review

Pathology of Diabetes-Induced Immune Dysfunction

Michael Alexander et al. Int J Mol Sci. .

Abstract

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.

Keywords: diabetes; immune dysfunction; immune senescence; infection; latent autoimmune diabetes in adults; medication side effects; vaccine uptake.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Diabetes-induced inflammaging pathway.
Figure 2
Figure 2
Various pathways of how hyperglycemia leads to senescence of immune cells in the bone marrow.
Figure 3
Figure 3
The pathways on how diabetes and aging both reduce response following vaccination. Arrows represent reduction.
Figure 4
Figure 4
The gut theory of latent autoimmune diabetes in adult (LADA) origin. Arrow represent “Increase”.

References

    1. Greenway F., Loveridge B., Grimes R.M., Tucker T.R., Alexander M., Hepford S.A., Fontenot J., Nobles-James C., Wilson C., Starr A.M., et al. Physiologic insulin resensitization as a treatment modality for insulin resistance pathophysiology. Int. J. Mol. Sci. 2022;23:1884. doi: 10.3390/ijms23031884. - DOI - PMC - PubMed
    1. Aluganti Narasimhulu C., Singla D.K. Mechanisms of COVID-19 pathogenesis in diabetes. Am. J. Physiol. Heart Circ. Physiol. 2022;323:H403–H420. doi: 10.1152/ajpheart.00204.2022. - DOI - PMC - PubMed
    1. Cuschieri S., Wilk P. Does pre-existing diabetes correlate with long COVID-19 in europe? Evidence from the analysis of the survey of health, ageing and retirement in europe’s corona surveys. J. Diabetes Res. 2024;2024:7459628. doi: 10.1155/2024/7459628. - DOI - PMC - PubMed
    1. Yang J.K., Feng Y., Yuan M.Y., Yuan S.Y., Fu H.J., Wu B.Y., Sun G.Z., Yang G.R., Zhang X.L., Wang L., et al. Plasma glucose levels and diabetes are independent predictors for mortality and morbidity in patients with sars. Diabet. Med. J. Br. Diabet. Assoc. 2006;23:623–628. doi: 10.1111/j.1464-5491.2006.01861.x. - DOI - PubMed
    1. Hulme K.D., Tong Z.W.M., Rowntree L.C., van de Sandt C.E., Ronacher K., Grant E.J., Dorey E.S., Gallo L.A., Gras S., Kedzierska K., et al. Increasing hba1c is associated with reduced cd8(+) t cell functionality in response to influenza virus in a tcr-dependent manner in individuals with diabetes mellitus. Cell Mol. Life Sci. 2024;81:35. doi: 10.1007/s00018-023-05010-4. - DOI - PMC - PubMed

LinkOut - more resources