目的探讨脱氢表雄酮（DHEA）对成骨细胞（oste0blasts，OB）及CD4+T细胞表达协同刺激分子的调控作用。方法颅骨酶解法培养鼠oB，体外模拟雌激素撤退；免疫磁珠细胞分选（rnag-c cell 9ort，MAC. S）法分离CD4+T细胞；将oB或CD4 T细胞分为对照组、E2及DHEA处理组，并以LPS刺激；以流式细胞术分析OB表面CDS0、CD86以及CD4+T细胞表面CD28、CⅡA4的表达。结果经E2及DHEA处理后，OB表达CDS0、CD86显著增加（P<0.05，P<0.01）；CsA可降低对照组及DHEA处理组OB CD80、CD86的表达（P<0.01）。除DHEA组CD28 T细胞百分比增加外（P<0.05），其余各组CD4 T细胞CD28和CIIA4的表达无显著改变（P>0.05）。结论DHEA可上调鼠OB协同刺激分子CDS0、O386表达，该作用可被CsA阻滞；DHEA还上调CD4 T细胞cD28的表达，提示可改善骨。免疫调节网络。

目的：探讨环孢素A（cyclosporin A, CsA）作用于人滋养层细胞差异表达的功能基因。方法：应用抑制性消减杂交筛选110μmol·L-1 CsA作用于JAR细胞系前后差异表达的功能基因，经RT2PCR及蛋白质印迹进一步验证CsA作用前后原代分离的人早孕期滋养层细胞及JAR细胞株titin 表达的变化。结果：CsA作用于人JAR细胞系前后出现6个具有差异表达的基因，其中1 个为已知基因titin，2个为功能未知的mRNA，3个为位于16号染色体上的EST。RT2PCR显示，CsA作用于人滋养层细胞24h后出现titin mRNA的表达，72h达高峰，并呈现明显的剂量依赖性，110μmol·L-1 CsA作用最明显。蛋白质印迹显示，CsA可诱导titin的表达。结论：CsA可能通过诱导滋养层细胞titin的高表达，改变其生物学行为,从而有利于胚胎着床及早期发育。

我们在以往研究中，引人选择性增强体液免疫效应的新型分子佐剂C3d。成功构建了重组避孕疫苗hCGlβ-C3d3，通过免疫Th2型优势的BALB/c小鼠和，Thl型优势的C57BL/6小鼠，显示分子佐剂C3d在不同品系小鼠均使免疫效应从Thl型细胞免疫向Th2型体液免疫偏倚[1-3]。

Chemokines and chemokine receptors have been implicated as pivotal players in many physiological and pathological situations, but little is known about the expression and function of chemokines and chemokine receptors at the materno-fetal interface. In this study, we first analyzed the transcription of 18 chemokine receptors in first-trimester human trophoblast cells. Among these receptors, CXCR4 was found highly transcribed. We demonstrated afterward that both CXCR4 and CXCL12 (stromal cell-derived factor-1; SDF-1) were expressed in trophoblast cells. Primary cultured trophoblast cells were also found secreting CXCL12 spontaneously. To identify the functional role of CXCR4/CXCL12 in these cells, we treated trophoblast cells with recombinant human (rh) SDF-1a and analyzed the cell viability and signaling pathway. The results showed that rhSDF-1a increased the viability of trophoblast cells and the activation of extracellular signal-regulated kinases signaling pathway in vitro. Our findings suggest that first-trimester trophoblast cells express functional CXCR4/CXCL12, which may play an important role in early pregnancy such as stimulating trophoblast cell proliferation or differentiation in an autocrine manner.

To show that an anti-human chorionic gonadotrophin-β (hCGβ) antibody response can be induced by inoculating Lb. Expressing hCGβ through diVerent mucosal pathways in mice of two strains, female BALB/c and C57BL/6 mice were immunized via vaginal, oral or nasal routes with 108, 109, and 1010 Lb.hCGβ (a recombinant Lactobacillus expressing hCGβ). The mice were immunized twice with a booster in study week 3. An indirect ELISA was used to determine anti-hCGβ IgG and IgA antibodies in vaginal lavage and serum, obtained from the 2nd to 8th week after the primary immunization. Flow cytometry was used to analyze the lymphocyte proliferation from these tissues, 1 week after the primary immunization. The hCGβ antigen-speciWc antibody-secreting cells of spleen, uterus, and vagina were evaluated by enzyme-linked immunospot assay (ELISpot), 2 weeks after the booster. The analysis showed that 109 and 1010 Lb.hCGβ inoculations induced similar anti-hCGβ antibody responses, while the three mucosal pathways induced similar antibody responses. The antiserum obtained after boosters with 109 and 1010 Lb. hCGβ was able to neutralize more than 100 ng/ml hCGβantigen, both in BALB/c and C57BL/6 mice. The highest antibody titer induced by vaginal mucosal immunization was stronger than that obtained via the other mucosal pathways. The B cells in the vagina appeared to proliferate after vaginal immunization (P <0.05). The numbers of anti-hCGβ IgG and IgA antibody-secreting cells in the uterus and vagina were greater than in the spleen. Therefore, the vaginal mucosal route appears to be a better immunization pathway to induce higher anti-hCGβ antibody levels in the reproductive tract.