Why Do Diabetic Patients Have Lower Immunity?
One of the most severe side effects of type II diabetes, a condition in which the body cannot produce or use insulin to break down blood sugar, is the impairment of the immune system. But if diabetes is primarily characterized by high circulating blood sugar levels, why does it lead to decreased immunity? Through in vitro and in vivo studies, researchers have identified the association between hyperglycemia, the suppression of cytokines, and the dysfunction of white blood cells, cells that combat pathogens in your bloodstream, to explain this phenomenon in diabetic patients. The elevated glucose levels lead to the suppression of interleukins, a type of cytokine or proteins that play an immunoregulatory role; consequently, with lower cytokine levels in diabetic individuals, the adaptive immune response, antibody production, and effector T-cell development is attenuated. Along with decreased interleukin levels, researchers also found that interferons, another type of cytokine whose role is to upregulate immune response, are suppressed in hyperglycemic individuals. From comparing experiments run on the white blood cells from healthy donors and diabetic individuals, researchers noticed that the leukocytes in the diabetic individuals expressed higher bacterial content, indicating that the capacity to stop bacterial proliferation is reduced in diabetic patients further harming immunity. Diseases and conditions, such as diabetes, obtain fascinating intricacies that can explain unintuitive and seemingly unrelated complications. Nevertheless, delving into the cellular and functional mechanisms of such diseases may shine a light on the immaculate balance and regulation of our body system, showcasing how the suppression of even just one kind of protein can lead to the deterioration of our health.
References
Afiat Berbudi, et al. “Type 2 Diabetes and Its Impact on the Immune System.” Current Diabetes Reviews, vol. 16, no. 5, Bentham Science Publishers, May 2020, pp. 442–449, https://doi.org/10.2174/1573399815666191024085838. Accessed 30 Sept. 2023.