The paucity of lymph node T cells (plt) mutation leads to a loss of CCL21 and CCL19 expression in secondary lymphoid organs. plt mice have defects in the migration of naive T cells and activated dendritic cells into the T cell zones of lymphoid organs, suggesting that they would have defects in T cell immune responses. We now demonstrate T cell responses in plt mice are delayed but ultimately enhanced. Responses to contact sensitization are decreased at day 2 after priming but increased at day 6. After subcutaneous immunization, antigen-specific T cell proliferation and cytokine production in plt mice are increased and remain markedly elevated for at least 8 wk. Compared with wild-type mice, a proportion of T cell response in plt mice are shifted to the spleen, and prior splenectomy reduces the T cell response in draining lymph nodes. After immunization of plt mice, T cells and dendritic cells colocalize in the superficial cortex of lymph nodes and in splenic bridging channels, but not in T cell zones. These results demonstrate that plt mice mount robust T cell responses despite the failure of naive T cells and activated dendritic cells to enter the thymus dependent areas of secondary lymphoid organs.
The tribological properties of trifluorotris(pentafluoroethyl) phosphate [(C 2 F 5 ) 3 PF 3 -, FAP]-derived ionic liquids were evaluated under boundary conditions. The anion is hydrophobic in comparison with bis(trifluoromethylsulfonyl)imide [(CF 3 SO 2 ) 2 N -, TFSI]. 1,3-Dialkyli midazolium salts of FAP provided much lower friction than 1,3-dialkylimidazolium salts of TFSI. In addition, the FAP salts exhibit better anti-wear properties than the TFSI salts. Another advantage of the FAP anion is availability of several cations to prepare ionic liquids. For example, tetraalkyl phosphonium, N,N-dialkylpyrrolidium, and tetramethylisouronium salts of FAP provided friction coefficient of approximately 0.1. Straight-chain carboxylic acids as model friction-reducing additives improved the tribological properties of the FAP salts. Surface analyses were conducted to study the boundary film formed by rubbing. It was found that the boundary film is composed of adsorbed anion on uppermost surfaces and reacted anion on sub-surfaces. The model friction-reducing additives were found on the rubbed surfaces.
Previously, we have shown a mutant mouse DDD/1 with T-cell–specific homing defect that is regulated by an autosomal recessive gene,plt (paucity of lymph node T cells), and seems to be caused by lymph node (LN) stromal cells. In the present study, immunohistochemical analysis showed unusual distribution of T cells in LN, Peyer's patches (PP), and spleen from plt/plt, probably due to the failure of T cells to migrate from blood into the T-cell zone in LN or PP, or into the spleen white pulp across high endothelial venule or marginal zone, respectively, based on the experiments in which labelled T cells were injected intravenously and detected in the tissues. Analysis of surface L-selectin and CD44 suggested that T cells with memory phenotype, probably from afferent lymphatics, recruit intoplt/plt LN. Linkage mapping by simple-sequence length polymorphism of genomic DNA from 190 backcross progenies produced by intercrossing with MSM/Ms, linked plt most closely with D4Mit237, and localized at 24.7 cM from cetromere on chromosome 4. We discuss the possibility that a wild-type gene on plt locus encodes a chemokine inducing T-cell–specific homing into peripheral lymphoid tissues.
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