Publications by authors named "Sarka Janusova"

T cells are pivotal in the adaptive immune defense, necessitating a delicate balance between robust response against infections and self-tolerance. Their activation involves intricate cross-talk among signaling pathways triggered by the T-cell antigen receptors (TCR) and co-stimulatory or inhibitory receptors. The molecular regulation of these complex signaling networks is still incompletely understood.

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Linker for activation of T cells (LAT) plays a key role in T-cell antigenic signaling in mammals. Accordingly, LAT orthologues were identified in the majority of vertebrates. However, LAT orthologues were not identified in most birds.

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Regulatory T cells (Tregs) are indispensable for maintaining self-tolerance by suppressing conventional T cells. On the other hand, Tregs promote tumor growth by inhibiting anticancer immunity. In this study, we identified that Tregs increase the quorum of self-reactive CD8 T cells required for the induction of experimental autoimmune diabetes in mice.

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The kinase LCK and CD4/CD8 co-receptors are crucial components of the T cell antigen receptor (TCR) signaling machinery, leading to key T cell fate decisions. Despite decades of research, the roles of CD4-LCK and CD8-LCK interactions in TCR triggering in vivo remain unknown. In this study, we created animal models expressing endogenous levels of modified LCK to resolve whether and how co-receptor-bound LCK drives TCR signaling.

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Mature T cells are selected for recognizing self-antigens with low to intermediate affinity in the thymus. Recently, the relative differences in self-reactivity among individual T-cell clones were appreciated as important factors regulating their fate and immune response, but the role of self-reactivity in T-cell biology is incompletely understood. We addressed the role of self-reactivity in T-cell diversity by generating an atlas of mouse peripheral CD8 T cells, which revealed two unconventional populations of antigen-inexperienced T cells.

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Article Synopsis
  • IL-17 plays a dual role in the immune system, offering protection against fungi and bacteria while also contributing to autoimmune diseases.
  • Researchers used a new mass spectrometry technique to analyze the IL-17 receptor (IL-17R) complex and discovered the linear ubiquitin chain assembly complex (LUBAC) as a key signaling component.
  • A crucial negative feedback loop involving the kinases TBK1 and IKKε was identified, which helps to terminate IL-17 signaling by modifying the adaptor ACT1 and releasing the ubiquitin ligase TRAF6, with NEMO having a unique role in negatively regulating this pathway.
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