RESUMEN
Allergic rhinitis (AR) is an inflammatory disorder of the nasal mucosa with high morbidity and prevalence. Natural killer (NK) cells might have a role in AR. We aimed to evaluate the changes of the markers and receptors on NK cells in AR patients compared to the non-atopic controls.Flow cytometric analysis was used with double staining of the Peripheral Blood Mononuclear Cells (PBMCs) to examine the expression of CD25 and CD69 markers, and NKG2D and NKG2A receptors on NK cells of 20 patients with AR and 20 non-atopic controls. The serum total IgE level was measured by Enzyme-linked Immunosorbent Assay.The expression of CD69 antigen on NK cells in AR patients was significantly higher than that of healthy group (p=0.03). No significant changes were observed between CD25, NKG2D and NKG2A expression on the surface of NK cells from healthy and AR subjects. Our study also showed that there was no significant correlation between the expression of CD69, CD25, NKG2D and NKG2A and level of serum total IgE in AR patients and normal subjects.These results indicated that the expression of CD69 antigen on NK cells of AR patients was increased. The high expression of CD69 on NK cells in AR patients suggested that these cells were activated, probably due to the cytokines secreted from allergen-stimulated T cells and activated monocytes.
Asunto(s)
Antígenos CD/genética , Antígenos de Diferenciación de Linfocitos T/genética , Expresión Génica/inmunología , Células Asesinas Naturales/inmunología , Lectinas Tipo C/genética , Rinitis Alérgica Perenne/genética , Adolescente , Adulto , Antígenos CD/inmunología , Antígenos de Diferenciación de Linfocitos T/inmunología , Biomarcadores/análisis , Estudios de Casos y Controles , Femenino , Humanos , Inmunoglobulina E/sangre , Subunidad alfa del Receptor de Interleucina-2/genética , Subunidad alfa del Receptor de Interleucina-2/inmunología , Células Asesinas Naturales/patología , Lectinas Tipo C/inmunología , Activación de Linfocitos , Masculino , Subfamília C de Receptores Similares a Lectina de Células NK/genética , Subfamília C de Receptores Similares a Lectina de Células NK/inmunología , Subfamilia K de Receptores Similares a Lectina de Células NK/genética , Subfamilia K de Receptores Similares a Lectina de Células NK/inmunología , Rinitis Alérgica , Rinitis Alérgica Perenne/inmunología , Rinitis Alérgica Perenne/patologíaRESUMEN
BACKGROUND: Type-I diabetes is an autoimmune inflammatory disease in which pancreatic beta-cells are selectively destroyed by infiltrating cells. TNF-related apoptosis-inducing ligand (TRAIL) is a type-II membrane protein of the TNF superfamily which is expressed in different tissues, including pancreas and lymphocytes. In humans, TRAIL interacts with four membrane receptors. TRAIL-R1 and TRAIL-R2 have cytoplasmic death domains, and can activate both caspases and NFkappaB pathways. The other two receptors, TRAIL-R3 and TRAIL-R4, are decoy receptors not capable of activating caspase cascade but may activate NF-kappaB and block apoptosis. As human beta cells are sensitive to TRAIL induced apoptosis, signaling via these molecules is considered to be a probable way of beta cell destruction. These molecules also are important in suppression of autorective T cells and immunoregulation. OBJECTIVE: To explore the importance of TRAIL and its receptors at pathogenesis of type-I diabetes, we compared expression of these molecules on T-cells of diabetic patients and healthy controls. METHODS: In this study, expression of TRAIL and its receptors at protein and mRNA levels were studied in freshly isolated peripheral T cells of 55 type I diabetic patients and 50 healthy individuals by flowcytometry, western blot and RT-PCR. RESULTS: We found that expression of TRAIL and its receptors in peripheral T-cells at both protein and mRNA levels are significantly increased in patients (except for TRAIL-R2 mRNA which was slightly higher in controls) but increase in TRAIL, TRAIL-R3 (2.7% vs. >0.5%) and TRAIL-R4 (2.6% vs. >0.5%) is more considerable. sTRAIL in sera of patients was significantly lower than in controls (P=0.01). CONCLUSION: Our results explain resistance of autoreactive T-cells to immunoregulatory mechanisms. Besides, increased expression of TRAIL in autoreactive T-cells may play an important role in beta-cell destruction. Lower level of sTRAIL in diabetic patients may be a reason for hyperactivation of autoreactive T-cells.
Asunto(s)
Diabetes Mellitus Tipo 1/metabolismo , Regulación de la Expresión Génica , Receptores del Ligando Inductor de Apoptosis Relacionado con TNF/metabolismo , Linfocitos T/metabolismo , Ligando Inductor de Apoptosis Relacionado con TNF/metabolismo , Adolescente , Adulto , Niño , Preescolar , Diabetes Mellitus Tipo 1/genética , Diabetes Mellitus Tipo 1/inmunología , Femenino , Humanos , Masculino , Persona de Mediana Edad , ARN Mensajero/genética , Receptores del Ligando Inductor de Apoptosis Relacionado con TNF/genética , Solubilidad , Ligando Inductor de Apoptosis Relacionado con TNF/genéticaRESUMEN
BACKGROUND: Apart from genetic and environmental factors, activation of autoreactive mechanisms has been proposed to play a role in the pathogenesis of schizophrenia. In recent years, considerable work has been carried out to understand the role and contribution of the immune system in this disease. OBJECTIVE: To investigate the T cell response to phytohaemagglutinin (PHA) and determine the serum levels of anti-nuclear antibody (ANA), anti-cytoplasmic antibody (ACA), and circulating immune complexes (CIC) in schizophrenic patients. METHODS: A total of 30 drug-free schizophrenic patients and 42 healthy controls were enrolled in this study. T cell proliferation in response to PHA was measured using Methyl Thiazol Tetrazolium test. ANA and ACA were measured by indirect immunofluorescence. CIC concentration was determined using poly ethylene glycol precipitation assay. RESULTS: Mean PHA response was 1.96 +/- 0.83 in patients and 3.72 +/- 1.39 in healthy controls (p< 0.001). ANA and CIC concentrations were not significantly different between two groups. In addition, ACA was detected only in patients. CONCLUSION: Increased production of ACA together with lower T cell response to mitogens in our patients provides evidence for the involvement of autoimmune mechanisms in the pathogenesis of schizophrenia.
