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ABSTRACT

Focusing on the father-child-relationship in a family systems perspective, this paper investigates longitudinal links of parenting, interparental conflict, and positive regard by both parents, to their emotional insecurity with father and mother. Furthermore, to clarify fathers’ contribution to children’s social development, aspects of the relationship to both parents are jointly considered. The sample was drawn from the German family panel pairfam and included 372 family triads with parents’ and children’s self-reports. Findings revealed consistent associations between interparental conflict and lack of positive regard and emotional insecurity, while parenting had no independent links with children’s emotional insecurity or social adjustment. Controlling for the stability of child outcomes, interparental conflict predicted children’s lower prosocial behavior and higher peer rejection. In addition, peer rejection was predicted by children’s emotional insecurity with father. The findings are in line with the emotional security hypothesis and highlight the importance of the father-child-relationship for developing positive peer relationships.  相似文献   
84.
BACKGROUND: Human studies have demonstrated that allergen immunotherapy induces memory suppressive responses and IL-10 production by allergen-specific T cells. Previously, we established a mouse model in which allergen immunotherapy was effective in the suppression of allergen-induced asthma manifestations. OBJECTIVE: In this study, we examined whether immunotherapy induces a long-lasting effect and investigated the role of IL-10 in successful immunotherapy. METHODS: Ovalbumin-sensitized BALB/c mice were treated with 3 injections of ovalbumin (1 mg, subcutaneous) on alternate days. After a short interval (1 week) and after a long interval (5 weeks), mice were challenged by ovalbumin inhalation, and subsequently, airway reactivity, airway eosinophilia, ovalbumin-specific IgE, and T(H)2 cytokine profile were measured. Flow cytometry and blocking of IL-10 receptors in vivo were used to gain insight in the role of IL-10 in the beneficial effects of allergen immunotherapy. RESULTS: After a long interval between ovalbumin immunotherapy and ovalbumin challenge, the development of airway eosinophilia and hyperresponsiveness to methacholine were as strongly suppressed as after a short interval. These suppressive effects coincided with significantly reduced serum ovalbumin-specific IgE levels and T(H)2 cytokine production. On immunotherapy, the IL-5:IL-10 ratio in the bronchoalveolar lavage fluid shifted toward IL-10. In ovalbumin-restimulated lung cell and thoracic lymph node cultures from these mice, IL-5 levels dramatically decreased, whereas the percentage of IL-10(+)CD4(+) T cells was not affected. Finally, in mice treated with mAb against IL-10 receptors, the beneficial effects of immunotherapy were largely abrogated. CONCLUSION: These data demonstrate that allergen immunotherapy induces a memory suppressive effect in which IL-10 is essential.  相似文献   
85.
类固醇激素合成急性调节蛋白(StAR)在胆固醇的代谢中发挥重要的作用。近期研究表明StAR同样表达于肝脏组织中,通过调节胆汁酸的合成,增加胆固醇的排泄。这为脂肪肝等脂类代谢异常类疾病的防治提供了一条新的途径。  相似文献   
86.
Generation and Regulation of CD8+ Regulatory T Cells   总被引:3,自引:0,他引:3  
Research into the suppressive activity of CD4+FoxP3+ T regulatory cells (Treg) has defined a sublineage of CD4+ cells that contribute to self-tolerance and resistance to autoimmune disease. Much less attention has been given to the potential contribution of regulatory sublineages of CD8+ cells. Analysis of a small fraction of CD8+ cells that target autoreactive CD4+ cells through recognition of the MHC class Ib molecule Qa-1 in mouse and HLA-E in human has revitalized interest in CD8+ Treg. Here we summarize recent progress and future directions of research into the role of this CD8+ sublineage in resistance to autoimmune disease. Cellular & Molecular Immunology. 2008; 5(6):401-406.  相似文献   
87.
Phenotypic characterization of regulatory CD4+CD25+ T cells in rats   总被引:8,自引:0,他引:8  
CD25 has become widely used as a marker for a subset of regulatory CD4(+) T cells present in the thymus and periphery of mice, rats and humans. However, CD25 is also expressed on conventionally activated T cells that are not regulatory and not all peripheral regulatory T cells express CD25. The identification of a stable and unique marker for regulatory T cells would therefore be valuable. This study provides a detailed account of the phenotype of CD4(+)CD25(+) regulatory T cells in rats. In the thymus, CD4(+)CD8(-)CD25(+) cells were found to have a more mature phenotype than the corresponding CD4(+)CD8(-)CD25(-) cells with respect to expression of Thy1 (CD90), CD53 and CD44, suggesting that CD25 expression, and perhaps commitment to regulatory function, might be a late event in thymocyte development. CD4(+)CD25(+) cells in both the thymus and periphery were found to have enriched and heterogeneous expression of activation markers such as OX40 (CD134) and OX48 (an antibody determined in this study to be specific for CD86). CD4(+)CD25(+) T cells were also found to have enriched expression of CD80, at both the mRNA and protein level. However, functional studies in vitro and in vivo showed that neither OX40 or CD86 were useful markers for the further subdivision of regulatory T cells. Our studies indicate that, at present, CD25 remains the most useful marker to enrich for regulatory CD4(+) T cells in rats and no further subdivision of the regulatory component of CD4(+)CD25(-)CD45RC(low) T cells has yet been achieved.  相似文献   
88.
Type I diabetes (T1D) is a T cell‐mediated autoimmune disease characterized by loss of tolerance to islet autoantigens, leading to the destruction of insulin‐producing beta cells. Peripheral tolerance to self is maintained in health through several regulatory mechanisms, including a population of CD4+CD25hi naturally occurring regulatory T cells (Tregs), defects in which could contribute to loss of self‐tolerance in patients with T1D. We have reported previously that near to T1D onset, patients demonstrate a reduced level of suppression by CD4+CD25hi Tregs of autologous CD4+CD25 responder cells. Here we demonstrate that this defective regulation is also present in subjects with long‐standing T1D (> 3 years duration; P = 0·009). No difference was observed in forkhead box P3 or CD127 expression on CD4+CD25hi T cells in patients with T1D that could account for this loss of suppression. Cross‐over co‐culture assays demonstrate a relative resistance to CD4+CD25hi Treg‐mediated suppression within the CD4+CD25 T cells in all patients tested (P = 0·002), while there appears to be heterogeneity in the functional ability of CD4+CD25hi Tregs from patients. In conclusion, this work demonstrates that defective regulation is a feature of T1D regardless of disease duration and that an impaired ability of responder T cells to be suppressed contributes to this defect.  相似文献   
89.
免疫耐受机制研究进展   总被引:1,自引:1,他引:1  
免疫耐受是机体免疫系统在接触某种抗原后所产生的对该抗原特异性免疫无应答状态,是免疫应答的一种特殊形式,免疫应答的复杂性决定了免疫耐受诱导的复杂性和困难性.随着免疫学的发展,人们对免疫耐受产生机制有了较多的认识.本文对免疫耐受与细胞凋亡、调节性T细胞及树突状细胞的研究进展进行综述.  相似文献   
90.
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