Elham Ashouri; Mohammad Hossein Dabbaghmanesh; Amirhossein Hadaegh; Soodeh Rowhanirad; Marizeh Bakhshayeshkaram; Gholamhossein Ranjbar Omrani
Abstract
Background: Killer cell immunoglobulin-like receptors (KIR) are expressed on NK cells and a subset of T cells. The variable KIR receptors along with their ligands, HLA class I, influence risk for autoimmune and malignant diseases. Objective: To investigate the KIR gene profiles in relation to susceptibility ...
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Background: Killer cell immunoglobulin-like receptors (KIR) are expressed on NK cells and a subset of T cells. The variable KIR receptors along with their ligands, HLA class I, influence risk for autoimmune and malignant diseases. Objective: To investigate the KIR gene profiles in relation to susceptibility to Graves’ disease in patients with ophthalmopathy. Methods: KIR genes profiles were analyzed in 90 patients presenting Graves’ disease with ophthalmopathy representing upper eyelid retraction, swelling, redness, conjunctivitis, and bulging eyes and were compared with the KIR gene profiles of 112 healthy controls. The presence and absence of 11 variable KIR genes were characterized using a gene-specific PCR typing system. Results: There was no significant difference in the distribution of KIR gene profiles between patients and controls. Conclusion: Our data show that none of the KIR genotypes contribute in susceptibility to Graves’ disease; although the role of HLA ligand remains to be characterized.
Ali Akbar Amirzargar; Abdol Ali Danesh; Farideh Khosravi; Mohammad Hossein Niknam; Behrouz Nikbin
Abstract
Background: Pulmonary tuberculosis (PTB) has recently become a major problem in developed countries especially in immune compromised HIV infected individuals. Cytokines, their genes and receptors have been implicated in the protective immunity, pathophysiology and development of tuberculosis. ...
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Background: Pulmonary tuberculosis (PTB) has recently become a major problem in developed countries especially in immune compromised HIV infected individuals. Cytokines, their genes and receptors have been implicated in the protective immunity, pathophysiology and development of tuberculosis. Material & Methods: In the present study the genotype frequencies of a number of polymorphic genes coding for cytokines or for cytokine receptors have been investigated in a case control study including a group of 40 Iranian PTB patients and 40 healthy individuals. The allelic polymorphism of cytokines SNPs were analyzed according to the protocols of the cytokine component designed for the 13th IHW by the Heidelberg University group. Using PCR-SSP method the following cytokine genes have been determined: IL-1 ¿ (T/C –889), IL-1¾ (C/T +3962), IL-1R (C/T pstI 1970), IL-1RA ( T/C mspaI 1100), IL-4RA (G/A +1902), IL- 12 (C/A –1188), TGF- ¾ (C/T codon 10, G/C codon 25), TNF-¿ (G/A –308, G/A –238), IL-2 (T/G –330 G/T +166), IL-4 (T/G –1098, T/C –590, T/C –33), IL-6 (G/C –174, G/A nt 560), IL-10 (G/A –1082, C/T –819, C/A –592). Results: From IL-1R cluster (pro- inflammatory cytokines) a positive significant association was found at position pstI 1970 C/T polymorphism where the C allele was over presented in the PTB patients (60% vs. 37.5%, P = 0.04). A significant negative association at codon 10 TGF- ¾ C/T polymorphism has also been shown in our patients, where the T allele was not detected in the patients but 10% of the control subjects expressed this allele (Fisher exact test, P = 0.05). At this codon allele T (Leucine substitution) is associated with high TGF- ¾ production. For TNF ¿ an insignificant tendency was found at position -308 A/G polymorphism where the G allele carried by 80% of cases and 65% of controls (P = 0.07). At position -238 a negative association was found at the GA polymorphism (10% vs. 25%, P = 0.07). For IL-6 an insignificant positive association at position -174 C/G polymorphism, G allele (57.5% vs. 37.5, P = 0.07) was found. At the other cytokine genes no specific association were found. Conclusion: In conclusion it is suggested that C allele at position pstI 1970 of IL-1 cluster increases and T allele at codon 10 of TGF- ¾ decreases in PTB patients.
