Jingxia Wu's research while affiliated with German Cancer Research Center and other places

Publications (8)

Article
T cells become functionally exhausted in tumors, limiting T cell–based immunotherapies. Although several transcription factors regulating the exhausted T (T ex ) cell differentiation are known, comparatively little is known about the regulators of T ex cell survival. Here, we reported that the regulator of G protein signaling 16 (Rgs-16) suppressed...
Article
Memory CD8+ T cells mature after antigen clearance and ultimately express CD8 protein at levels higher than those detected in effector CD8+ T cells. However, it is not clear whether engagement of CD8 in the absence of antigenic stimulation will result in the functional activation of T cells. Here, we found that CD8 antibody‐mediated activation of m...
Article
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CD8 ⁺ T cells become functionally impaired or “exhausted” in chronic infections, accompanied by unwanted body weight reduction and muscle mass loss. Whether muscle regulates T cell exhaustion remains incompletely understood. We report that mouse skeletal muscle increased interleukin (IL)–15 production during LCMV clone 13 chronic infection. Muscle-...
Article
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T cell factor 1 (Tcf1) promotes the central memory CD8⁺ T (TCM) cell differentiation and stemness in lymphoid tissues after systemic infections. It remains unclear whether Tcf1 regulates the CD103high tissue-resident memory CD8⁺ T (TRM) cell formation in non-lymphoid tissues after mucosal infections. We find that Tcf1 is progressively decreased dur...
Article
To maintain immune tolerance, effector T cell (Teff) responses must be checked by the regulatory T cells (Tregs) in time. It remains incompletely understood how Tregs sense real‐time effector T cell activation. Here, we report that the AP‐1 transcription factor JunB, which is induced in Teffs upon T cell receptor (TCR) activation, is also increased...
Article
Patients with the neurological disorder HSAN-I suffer frequent infections, attributed to a lack of pain sensation and failure to seek care for minor injuries. Whether protective CD8 ⁺ T cells are affected in HSAN-I patients remains unknown. Here, we report that HSAN-I-associated mutations in serine palmitoyltransferase subunit SPTLC2 dampened human...
Article
HIV-1 Nef is a multifunctional protein that optimizes virus spread and promotes immune evasion of infected cells to accelerate disease progression in AIDS patients. As one of its activities, Nef reduces the motility of infected CD4+ T lymphocytes in confined space. In vivo, Nef restricts T lymphocyte homing to lymph nodes as it reduces the ability...
Article
Full-text available
Treatment of type 2 diabetes mellitus continues to pose an important clinical challenge, with most existing therapies lacking demonstrable ability to improve cardiovascular outcomes. The atheroprotective peptide apelin (APLN) enhances glucose utilization and improves insulin sensitivity. However, the mechanism of these effects remains poorly define...

Citations

... IL-15 was also analyzed, since it is a pleiotropic cytokine with a broad spectrum of biological functions that can act in an inflammatory or antiinflammatory manner, depending on the context (39,40). Interestingly, IL-15 has been reported to be secreted by muscle cells under homeostatic as well as pathological conditions (41,42) and little is known about its role in T. cruzi infection. Examination of serum IL-15 showed a slight increase at 15 dpi compared to n.i. ...
... Recently, it has been demonstrated that TCF1 binds to the Itgae locus and inhibits CD103 expression. 96 Using a global gene expression analysis of Tcf7 sufficient and Tcf7 deficient P14 CD8 + T cells, WU et al reported an increased expression of CD103 in Tcf7 deficient cells associated with a decreased expression of tissue egress genes such as Sell and Ccr7. 96 Finally, Bhlhe40 is another TF that has been recently described. ...
... JUNB is a key transcriptional regulator of T cell differentiation [14,15], macrophage activation [13] as well as a well-known inhibitor of granulocyte progenitor proliferation [19]. Characterization of the immune cell landscape in JUNB-deficient mice revealed that the metastatic phenotype in stromal JUNB KO mice does not correspond to the increased antitumor response observed in regulatory T cell-specific JUNB knockout mice [39,40]. Moreover, as the observed effect on T cell infiltration was visible in the primary tumor rather than the early metastatic lungs, we reasoned that enhanced metastasis is most likely not due to altered T cell infiltration and focused on myeloid cells in the tumor microenvironment instead. ...
... mTORC1 inhibition combined with CTLA4 blockade before CD8 + T cell priming cooperates to promote memory differentiation associated with enhanced vaccine responses 83 . Conversely, sustained mTORC1 activation, such as that observed in patients lacking the key enzyme in sphingolipid biosynthesis (SPTLC2), or hyperactivating mutations in PI3Kδ subunits (which cause activated PI3Kδ syndrome), experience recurrent infections and poor immune recall responses 84,85 . Interestingly, signalling through PD1, another co-inhibitory receptor, on activated CD8 + T cells decreased glycolysis and increased fatty acid oxidation of endogenous lipids via upregulation of CPT1α 86 . ...
... Moreover, a highthroughput assay utilizing pressure waves induced by pico-second laser pulse (Yoshikawa et al, 2011;Burk et al, 2015) revealed a significant reduction of the critical pressure for detachment in GPR56 KD vs. control conditions (Appendix Fig S2D). In addition, we estimated the active deformation of cells by tracing the cell periphery over time (Burk et al, 2015;Lamas-Murua et al, 2018), which was significantly reduced in GPR56 KD vs control cells ( Fig 2G). In summary, these studies provided strong evidence for a functional role of GPR56 in healthy and leukemic HSPCs and confirmed a major impact of GPR56 on the adhesion and deformation capacity of human leukemic cells. ...
... 24 It was initially identified as a hormone secreted from adipose tissue, 25 but also secreted by skeletal muscle 26 and other tissues. 27,28 Apelin activates Ga q and stimulates phospholipase C, which triggers inositol triphosphate (IP3) release and elevates intracellular Ca 2+ levels. 29 Enhanced intracellular Ca 2+ levels is known to enhance muscle-based thermogenesis. ...