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peripheral tolerance
First, this process may be integral in the clonal deletion of self-reactive lymphocytes and maintenance of peripheral tolerance.
      
These studies suggest that the underlying mechanisms of peripheral tolerance include deletion, anergy, immune deviation, and regulatory T cells.
      
Additionally, IL-6 released by dendritic cells (DCs) inhibits the suppressive function of CD4+CD25+ T-regulatory cells, thus inhibiting the peripheral tolerance.
      
These approaches included induction of peripheral tolerance, immunotoxin targeting of activated T cells, and cytokine manipulations.
      
By understanding the mechanisms of peripheral tolerance and the reasons they fail in autoimmunity, we may learn how to prevent undersirable autoimmunity and how to encourage an autoimmune response when it is needed to eliminate tumor cells.
      
Findings and perspectives gained through the study of peripheral tolerance in our model, as well as relevant observations from the literature, will be reviewed.
      
Through the use of mice expressing transgenic T-cell receptors specific for foreign antigens, we have concluded that the separable mechanisms of anergy and active suppression by CD25+T cells work in concert to produce peripheral tolerance.
      
Through discussion of these observations, we have developed a historical perspective on recent advances in the understanding of mechanisms of peripheral tolerance.
      
Transgenic studies demonstrated that the dysregulation of LIGHT activity results in the disturbance of T-cell homeostasis and ultimately the breakdown of peripheral tolerance.
      
Mechanisms of central and peripheral tolerance have evolved to control effector cells that could respond to autoantigens.
      
We succeeded to induce peripheral tolerance to this AA-associated T cell epitope following nasal administration of a peptide containing this epitope (mycobacterial hsp60 176-190).
      
While some protocols are effective in inducing peripheral tolerance in experimental animals, these regimens are at present not yet applicable in the clinical situation.
      
Maternal immune aggression directed against the fetus is partly inhibited by peripheral tolerance mechanisms that act locally to deplete cells capable of attacking the fetus.
      
T-helper cell intrinsic defects in lupus that break peripheral tolerance to nuclear autoantigens
      
Fas is a pro-apoptotic molecule involved in activation-induced cell-death of T?lymphocytes, central and peripheral tolerance and immune privilege.
      
PD-1 gene-deficient mice developed autoimmune diseases, which early led to the hypothesis of PD-L1 regulating peripheral tolerance.
      
These findings suggest that 3H1-CpG vaccinations can break peripheral tolerance to CEA and induce protective antitumor immunity in this murine model transgenic for human CEA.
      
Obstacles for a general blockade of PD-L1 might be its role in mediating peripheral tolerance.
      
Along with cell death induced by growth factor deprivation, AICD followed by the elimination of useless or potentially harmful cells preserves homeostasis, leads to the termination of cellular immune responses and ensures peripheral tolerance.
      
First, they have provided key information on tolerance mechanisms, both on the deletion of T cells in the thymus and on the induction of peripheral tolerance by anergy and apoptosis.
      
 

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