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1.
IJI-Iranian Journal of Immunology. 2004; 1 (3): 169-176
in English | IMEMR | ID: emr-174291

ABSTRACT

Background: The effectiveness of T cell vaccination has been demonstrated in a variety of animal models of both induced and spontaneous autoimmune diseases. The purpose of this study was to test the T cell vaccination protocol to treat and prevent collagen induced arthritis [CIA] in a rheumatoid arthritis model


Methods: CIA was induced by an intradermal injection of an artheritogen substance at the right paw of each female Albino rat under ether anesthesia. T cells were achieved from spleens of syngeneic rats that developed full clinical features of CIA. Rats suffering from CIA were divided in case groups [4 rats/group] based on the degrees of their disease and were injected intraperitoneally once with a suspension of T cells to investigate the effects of autoreactive T cells on CIA. To investigate the preventive effects of autoreactive T cells on CIA, 12 normal rats were injected intraperitoneally once either with a suspension of T cells or PBS, respectively. The results were evaluated by clinical observation, histopathological and radiographic findings


Results: Intraperitoneal inoculation of T cells to rats suffering from CIA, suppressed the development of CIA in case rats in stage 2 of the disease but not the other case rats. Rats who received T cells as prevention, showed the mild signs of disease. Injection of artheritogen substance to the case rats didn't result in development of CIA but the control rats, showed signs of CIA


Conclusion: The results of this pilot study demonstrate that CIA presentations and signs can be subsided or suppressed by autoreactive T cells. The vaccination is most effective before onset of the disease and in early phases of CIA. Modifying and improving the protocol using more cases is recommended

2.
Iranian Journal of Diabetes and Lipid Disorders. 2004; 3 (2): 107-111
in Persian | IMEMR | ID: emr-203802

ABSTRACT

Background: type 1A Diabetes Mellitus [T1DM] is a chronic and progressive auto- immune disorder resulting from immune mediated destruction of Langerhans islet beta cells. The etiology of T1DM like the other autoimmune diseases is unknown and many factors are involved, both humoral and cell-mediated immunity have a critical role in T1DM pathogenesis. The cytokines, the immunomodulatory peptides, are responsible for the immune cell recruitment and producing auto-antibodies by the immune effector cells. To evaluate the role of cytokines in sensitivity or resistance to T1DM, we have employed IFN gamma to determine their gene polymorphisms and their association with T1DM


Methods: 30 patient suffering from T1DM and 40 normal control were studied simultaneously .PCR technique was used to characterize the polymorphisms of cytokine. Salting out method was performed for DNA isolation. The polymorphosime of IFN gamma gene was determined on position UTR+5664`5.The PCR products were evaluated by Gel Electerophoresis Technique


Results: there was a significant difference between patient and control group in TT allele IFN gamma gene: p<0.05, RR: 0.39[0.22

Conclusion: in this study, we found a negative association between IFN gamma gene at position 5'UTR+5644 and T1DM in study group that means this allele may be a protective factor against T1DM

3.
IJI-Iranian Journal of Immunology. 2004; 1 (2): 130-132
in English | IMEMR | ID: emr-66025

ABSTRACT

Type 1 Diabetes [T1D] is a chronic and progressive autoimmune disorder. Cytokines play a critical role in the pathogenesis of T1D. IFN- polymorphism was investigated in T1D and compared with normal controls. Thirty patients suffering fromT1D and 40 normal controls were studied simultaneously using PCR technique. IFN- gene was evaluated at position 5'UTR +5644. There was a significant difference between patient and control groups in TT genotype [P<0.05]. In this study, we found a negative association between IFN- gene at position 5'UTR +5644 and T1D in Iranian patients pointing to T allele as a protective factor against T1D


Subject(s)
Humans , Male , Female , Cytokines/genetics , Genes , Polymorphism, Genetic
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