Moazezi Z.,Babol University of Medical Sciences |
Hosseinian A.,Babol University of Medical Sciences |
Moazam E.A.,Babol University of Medical Sciences |
Eslami M.-B.,Tehran University of Medical Sciences |
And 5 more authors.
Iranian Journal of Allergy, Asthma and Immunology | Year: 2014
It has been widely thought that diabetic patients are prone to infections due to hyperglycemia induced immunodeficiency; the present study was designed to examine this opinion. In diabetic patients and normal control groups T-cell reactivity to hsp-60 molecule, tetanus toxoid recall antigen (TT) and phytohemagglutinin-A (PHA) mitogen were evaluated The number of circulating IFN-γ, IL-10 and IL-13 cytokine producing cells stimulated with above antigens or mitogen as well as the serum levels of Th1/Th2 type cytokines were determined. Total serum immunoglobulins (IgG, IgA, IgM), C3, C4 and CH50 were also measured. Diabetic patients showed a positive circulating T-cell reactivity to human recombinant hsp60 However, this reactivity was significantly lower in comparison to control group (p<0.001). All other examined factors were not significantly different between diabetic and normal subjects except for the number of IFN-γ and IL-13 producing cells in response to PHA stimulation, which was higher in control gtroup (p=0.006, 0.018, respectively). The mean serum concentration of IgA in diabetic patients was 245.86±115.05 mg/dl versus 192.96±105.33 mg/dl in healthy control group (p<0.018). We were not able to demonstrate any substantial mitigation in cellular arms of immune reaction to some prominent T-cell antigens and mitogens, as well as, in main parameters of humoral immunity of diabetic patients, thus, the common notion of believing that patients with diabetes suffering from immunodeficiency should be revised. It is much more appropriate that "altered immunity" is applied instead of "immunodeficiency" to explain the immunity condition in this group of patients. Copyright© Spring 2014, Iran J Allergy Asthma Immunol. All rights reserved. Source