Author/Authors :
Moazezi, Zoleikha Department of Endocrinology - Ayatollah Rohani Hospital - Babol University of Medical Sciences, Babol , Hosseinian, Azam Department of Endocrinology - Ayatollah Rohani Hospital - Babol University of Medical Sciences, Babol , Ahmad Moazam, Ensiyeh Department of Endocrinology - Ayatollah Rohani Hospital - Babol University of Medical Sciences, Babol , Eslami, Mohamed-Bagher Department of Pathobiology - Faculty of Health - Tehran University of Medical Sciences, Tehran , Mosavi, Ezatollah Department of Microbiology and Immunology - Faculty of Medicine - Babol University of Medical Sciences, Babol , Akhavan-Niaki, Haleh Cellular and Molecular Biology Research Center - Babol University of Medical Sciences, Babol , Bijani, Ali Non- Communicable Pediatrics Diseases Research Center - Babol University of Medical Sciences, Babol , Schloot, Nanette Department of Immunobiology - German Diabetes Research Center, Dusseldorf, Germany , Mostafazadeh, Amrollah Cellular and Molecular Biology Research Center - Babol University of Medical Sciences, Babol
Abstract :
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-', 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-' 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.
Keywords :
Adaptive Immunity , Complement System Proteins , Cytokines , Diabetes Mellitus , Infection