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Objective To evaluate the effect of γ-aminobutyric acid (GABA) and its receptors upon the proliferation of CD8+T cells.Methods The splenic CD8+T cells of Balb/c mice were obtained by CD8+f cell magnetic bead sorting kit.Under the effect of CD3/CD28-activated magnetic bead,CD8+T cells were stimulated by different concentrations of GABA.5-bromo-2-deoxyuridine (BrdU) labeling and flow cytometry were performed to detect the proliferation of CD8+T cells.The expression levels of GABA-A and GABA-B receptor before and after CD8+T cell activation were compared by fluorescent quantitative real-time polymerase chain reaction (PCR).Result Flow cytometry result revealed that GABA could inhibit the proliferation of activated CD8+T cells,manifested as significant decrease in the quantity of CD152+CD8+T cells.Fluorescent quantitative real-time PCR demonstrated that GABA-A receptor subtypes α2,α6 and GABA-B receptor subtype 1a were expressed only when the CD8+T cells were activated.After CD8+T cell activation,the quantity of GABA-A receptor subtypes α3,αs,β2,β3,γ1,γ2 and θ were significantly increased,whereas the quantity of GABA-B2R and GABA-B1b did not significantly differ before and after CD8+T cell activation.Conclusions GABA can suppress the proliferation of activated CD8+T cells.The activation of CD8+T cells is regulated by GABA receptors.However,the underlying mechanism remains to be elucidated.
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Objectives To explore polymorphisms of CD152 gene promoters (-1722T/C,-1661A/G) and exon1 (+49A/G) in children with idiopathic ischemic stroke and assess the association between these polymorphisms with the disease. Methods Us-ing the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method, polymorphisms in the CD152 exon1 region (+49A/G) and promoter regions (-1722T/C,-1661A/G) were genotyped in 51 Han children with idiopathic ischemic stroke and 74 healthy Han children. Results The CD152 genotypes in control group and idiopathic ischemic stroke children were consistent to principle of Hardy-Weinberg Equilibrium (HWE) byχ2 test. The CD152+49GG genotypes and G allele frequency in the patients showed a signiifcant increase compared to the controls (χ2=7.053, 6.351, P0.05). Clinical features (hemi-paresis, dysarthria, seizures, consciousness change, and preceding infections) did not show signiifcant correlation with genotypes and frequency of the CD152+49 polymorphisms in children with idiopathic ischemic stroke (P>0.05). Conclusions The CD152+49A/G polymorphisms may relate to idiopathic ischemic stroke.
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Leprosy is a spectral disease exhibiting two polar sides, namely, lepromatous leprosy (LL) characterised by impaired T-cell responses and tuberculoid leprosy in which T-cell responses are strong. Proper T-cell activation requires signalling through costimulatory molecules expressed by antigen presenting cells and their ligands on T-cells. We studied the influence of costimulatory molecules on the immune responses of subjects along the leprosy spectrum. The expression of the costimulatory molecules was evaluated in in vitro-stimulated peripheral blood mononuclear cells of lepromatous and tuberculoid patients and healthy exposed individuals (contacts). We show that LL patients have defective monocyte CD86 expression, which likely contributes to the impairment of the antigen presentation process and to patients anergy. Accordingly, CD86 but not CD80 blockade inhibited the lymphoproliferative response to Mycobacterium leprae. Consistent with the LL anergy, there was reduced expression of the positive signalling costimulatory molecules CD28 and CD86 on the T-cells in these patients. In contrast, tuberculoid leprosy patients displayed increased expression of the negative signalling molecules CD152 and programmed death-1 (PD-1), which represents a probable means of modulating an exacerbated immune response and avoiding immunopathology. Notably, the contacts exhibited proper CD86 and CD28 expression but not exacerbated CD152 or PD-1 expression, suggesting that they tend to develop a balanced immunity without requiring immunosuppressive costimulatory signalling.
Assuntos
Adulto , Feminino , Humanos , Masculino , /imunologia , /imunologia , /imunologia , Hanseníase/microbiologia , Mycobacterium leprae/imunologia , Receptor de Morte Celular Programada 1/imunologia , Linfócitos T/imunologia , /metabolismo , /metabolismo , /metabolismo , Estudos de Casos e Controles , Interações Hospedeiro-Parasita , Hanseníase/imunologia , Mycobacterium leprae/fisiologia , Receptor de Morte Celular Programada 1/metabolismoRESUMO
Objective To investigate the significance of B7-CD28/CTLA-4 (CD152),co-stimulatory molecules of T lymphocytes,in the onset,development and prognosis of genital congdyloma acuminatum (CA) in females.Methods Flow cytometry was utilized to detect the expression levels of CD80/CD86 in peripheral blood lymphocytes and of CD28/CD152 (CTLA-4) in CD4~+/CD8~+ T lymphocytes from 30 CA patients (17 primary CA,13 recurrent CA,15 at recovery stage of CA) and 15 healthy volunteers as con- trols.Results No significant difference was found for the frequencies of CD80~+,CD86~+,CD4~+/CD28~+ and CD8~+/CD28~+ lymphocytes between the primary or recurrent group and the control group.The frequencies of CD8~+/CD28~+,CD4~+/CD28~+ and CD80~+ lymphocytes were significantly higher in the recovery group than those in the recurrent group (P0.05).Conclusions There is an abnormal expression of co-stimulatory molecules B7-CD28/CTLA-4 (CD152) in periphoral blood lym- phocytes,CD4~+ and CD8~+ T lymphocytes in female patients with genital CA,and the expression abnormaility is closely linked with different disease stages of CA.