Sensors, and Epigenetic Imprinting Cell Anergy: Anergy Factors, Avoidance New Insights into the Molecular Basis of T
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Signaling through CD28 and CTLA-4 controls two distinct forms of T cell anergy.
Primary T cell proliferative responses to TCR ligation plus CD28 costimulation are surprisingly heterogeneous. Many cells that enter G1 fail to progress further through the cell cycle, and some of these cells subsequently fail to divide upon restimulation, even in the presence of IL-2. Such IL-2-refractory anergy is distinct from the IL-2-reversible anergy induced by TCR occupancy in the absenc...
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Leprosy is a model disease for understanding human immune responses underlying diseases caused by intracellular pathogens, as well as providing valuable insights into autoimmune disorders and cancer. This review addresses the unresponsiveness/anergy of host T cells to the causative pathogen Mycobacterium leprae and describes both the adaptive and innate immune responses observed during the clin...
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Tumors can escape from immunity by repressing leukocyte adhesion molecule expression on tumor endothelial cells and by rendering endothelial cells unresponsive to inflammatory activation. This endothelial cell anergy is induced by angiogenic growth factors and results in reduced leukocyte-vessel wall interactions, thereby attenuating infiltration of leukocytes into the tumor. This report descri...
متن کاملNdrg1 is a T-cell clonal anergy factor negatively regulated by CD28 costimulation and interleukin-2
Induction of T-cell clonal anergy involves serial activation of transcription factors, including NFAT and Egr2/3. However, downstream effector mechanisms of these transcription factors are not fully understood yet. Here we identify Ndrg1 as an anergy factor induced by Egr2. Ndrg1 is upregulated by anergic signalling and maintained at high levels in resting anergic T cells. Overexpression of Ndr...
متن کاملInhibition of cell cycle progression by rapamycin induces T cell clonal anergy even in the presence of costimulation.
Costimulation (signal 2) has been proposed to inhibit the induction of T cell clonal anergy by either directly antagonizing negative signals arising from TCR engagement (signal 1) or by synergizing with signal 1 to produce IL-2, which in turn leads to proliferation and dilution of negative regulatory factors. To better define the cellular events that lead to the induction of anergy, we used the...
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تاریخ انتشار 2009