OBJECTIVE To evaluate the effect of antiviral agents in treating of severe acute respiratory syndrome(SARS). METHODS Based on the particular data (including medical history,examiuations and treatments) of 1702 patients of with SARS which were offered by the Health Bureau of Guangdong Province,the inpact factors of death and the course of diseases of SARS were retrospectively analyzed with unifactorial and multifactors statistic analysis methods. RESULTS It did not show any signs that the death rate could be decreased by the six antiviral agents in common use,but vidarabine could help to shorten the course of disease(OR=1.399,P=0.025),while oseltamivir might be prolonged the course of disease(OR=0.708,P=0.000). CONCLUSIONS The data showed that the effect of the six antiviral agents for curing SARS is limited,and a new antiviral treatment for SARS should be explored further.

Objective To explore the role of dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin (DC-SIGN) in the tubulointerstitial lesions of immune-mediated nephrotoxic nephritis (NTN) and the intervention regulation by anti-P-selectin lectin-EGF domain monoclonal antibody (PsL-EGFmAb). Methods WKY rats were randomly divided into control,NTN and PsL-EGFmAb-treated groups. The mrs in NTN group were injected with 1 ml nephrotoxic rabbit serum per kilogram of rat body weight; the ones in PsL-EGFmAb-treated group were injected with 2 mg PsL-EGFmAb per kilogram of rat body weight simultaneously and 2 h later after nephrotoxic rabbit serum injection; and those in control group were injected with equal volume of 0.9% saline. Renal function and pathology were observed at day 4, 7 and 14 after the induction of NTN. Distribution of DC-SIGN + dendritic cells (DCs) in renal tissues was measured by immunofluorescence. Real-time PCR was performed to examine the expression of P-selectin,RANTES, TNF-α, IL-10, IFN-γ and IL-4. Expression of MHC Ⅱ , CD80 and DC-SIGN on dendritic cells was analyzed by flow cytometry. Transendothelial migration was used to detect the ability of DCs migration. DCs ability to activate T cells was determined by mixed lymphocyte reaction (MLR). ELISA was used to detect the concentration of IFN-γ and IL-4 in the supernatant of MLR. Results At day 4, immature DC-SIGN+ DCs infiltrated the rat renal tubulointerstium of NTN group, matured at day 14, and enhanced the ability to migrate and activate T cells. The distribution of DC-SIGN + DCs was significantly related to the form of crescent, tubulointerstial lesions and renal function. In addition, expression of chemokine RANTES and proinflammatory cytokine TNF-α continuously augmented since day 4, while anti-inflammatory eytokine IL-10 decreased after markedly increased at day 4. At day 14, IFN-γ/IL-4 mRNA increased, which was obviously related to DCs maturation. The intervention of PsL-EGFmAb supressed the expression of DC-SIGN and CD80 on DCs, depressed DCs maturation, migration and ability to activate T cells,down-regulated proinflammatory cytokines and up-regulated anti-inflammatory cytokines in kidney,and thus regulated Th1/Th2 bias. At the same time, kidneys showed the decrease of crescents,improvement of tnbulointerstium damage and renal function. Conclusions DC-SIGN may mediate DCs tubulointerstitial infiltration. It may be also a potent regulator of local immune reaction imbalance and pathology of tubulointerstium. PsL-EGFmAb may depress DCs migration and downregulate DCs maturation and function through DC-SIGN, and thus having a role in prevention and treatment.

Objective:To explore the effect of leptin on B cells in patients with systemic lupus erythematosus (SLE).Methods:Peripheral blood mononuclear cells (PBMCs) were isolated from SLE patients, and then CD19 + B cells were purified with magnetic bead sorting method. PBMCs or purified B cells were cultured with recombinant leptin at 0, 100, 250 ng/ml for 3 or 5 days. The frequencies of plasma cells, follicular helper T (Tfh) cells and peripheral helper T (Tph) cells, as well as activation markers (CD80, CD86) and leptin receptor and the proliferation of B cells were determined with flow cytometry. The concentrations of antibodies and cytokines were examined with enzyme-linked immunosorbnent assay (ELISA). Data were analyzed with t test and analysis of variance (ANOVA). Results:Increased levels of leptin were positively correlated with systematic lupus erythematosus disease activity index (SLEDAI) and the frequency of plasma cells in SLE patients. Leptin receptor could be detected on SLE B cells, and recombinant leptin elevated the levels of its receptor on CD19 + B cells [(7.8±1.3)% vs (6.1±0.9)%, t=3.36, P=0.006]. Leptin enhanced the expression of CD80 [(21±4)% vs (19±4)%, t=2.84, P=0.004] and CD86 [(22±4)% vs (19±4)%, t=4.92, P=0.004] on SLE B cells in vitro. It also promoted B cells to differentiate into plasma cells [(7.6±1.5)% vs (5.2±1.3)%, t=6.42, P=0.025]. There was no statistical significant difference of the effect of leptin on B cell proliferation. Leptin also increased the levels of antibodies [IgG: (62±3) ng/ml vs (45±4) ng/ml, t=7.75, P<0.001; IgM: (112±24) ng/ml vs (56±18) ng/ml, t=5.38, P<0.001] and inflammatory cytokines [IL-6: (24±5) pg/ml vs (20±5) pg/ml, t=4.09, P=0.002; TNF-α: (19.1±3.8) pg/ml vs (14.1±2.9) pg/ml, t=3.38, P=0.006; IL-10: (24±5) pg/ml vs (20±5) pg/ml, t=4.09, P=0.002] secreted by B cells. In addition, leptin significantly upregulated the frequencies of Tfh cells[(2.82±0.49)% vs (1.28±0.20)%, t=4.56, P=0.001] and Tph cells [(4.5±0.5)% vs (3.4±0.4)%, t=3.88, P=0.003]. Conclusion:Leptin could directly promote the activation, differentiation and secretory capacity of B cells by binding to its receptor, and also modulate B cell responses indirectly via enhancement of Tfh and Tph cells, which may be involved in the pathogenesis of SLE.