An emerging family of innate lymphoid cells (termed ILCs) has an essential role in the initiation and regulation of inflammation. However, it is still unclear how ILCs are regulated in the duration of intestinal inflammation. Here, we identify a regulatory subpopulation of ILCs (called ILCregs) that exists in the gut and harbors a unique gene identity that is distinct from that of ILCs or regulatory T cells (Tregs). During inflammatory stimulation, ILCregs can be induced in the intestine and suppress the activation of ILC1s and ILC3s via secretion of IL-10, leading to protection against innate intestinal inflammation. Moreover, TGF-β1 is induced by ILCregs during the innate intestinal inflammation, and autocrine TGF-β1 sustains the maintenance and expansion of ILCregs. Therefore, ILCregs play an inhibitory role in the innate immune response, favoring the resolution of intestinal inflammation.

Innate lymphoid cells (ILCs) reside in mucosal surfaces to potentiate immune responses, sustain mucosal integrity and maintain tissue homeostasis. However, how tumor infiltrating ILCs modulate tumor development and progression is unclear. Here we profiled tumor infiltrating ILCs during colorectal cancer (CRC) progression by single-cell RNA sequencing. We identified six clusters of tumor infiltrating ILCs with unique features. ILC1s expressed inhibitory receptors and underwent inhibitory functional conversion at the late stage of CRC. ILC2s were classified into three subsets (called ILC2-A,-B,-C), of which ILC2-C subset could facilitate tumor progression. HS3ST1 and PD1 were highly expressed in ILC2s of late stage CRC tumors and deficiency of HS3ST1 or PD1 in ILC2s suppressed tumor growth. Moreover, ILC3s transdifferentiated into ILCregs during CRC progression and ILCregs promoted tumor growth. Of note, TGF-β signaling initiated the conversion of ILC3s to ILCregs and blockade of TGF-β signaling could disrupt the ILCreg transdifferentiation and inhibited tumor growth. Thus, intervention of ILC conversions might be a potential strategy for CRC immunotherapy.

The COVID-19 epidemic has caused increasing public panic and mental health stress. In this study, we explore the prevalence and factors linked to anxiety and depression in hospitalized patients with COVID-19. A total of 144 patients diagnosed with COVID-19 underwent depression and anxiety assessment by using the Hospital Anxiety and Depression Scale (HADS). Social support level was also evaluated by the Perceived Social Support Scale (PSSS) at admission. Results showed that gender, age, oxygen saturation, and social support were associated with anxiety for COVID-19 patients. In addition, age, family infection with SARS-CoV-2, and social support were the risk factors associated with depression. Moreover, we designed a psychological–behavioral intervention (PBI) program that included psychological support and breathing exercises, and explored its effects on patients with COVID-19. Of the 144 participants, 26 patients with both anxiety and depression symptoms (cutoff score of ≥8 on HADS-A and HADS-D) were randomly assigned to the intervention group and the control group at a 1:1 ratio. After 10-day treatment, the HADS scores of depression and anxiety were significantly reduced in the intervention group, and PSSS scores were also significantly improved. However, no significant differences in HADS and PSSS scores between pre- and post-treatment were found in the control group. Our findings indicate that mental concern and appropriate intervention are essential parts of clinical care for COVID-19 patients.

The maize (Zea mays) gibberellin (GA)-deficient mutant dwarf1 (d1) displays dwarfism and andromonoecy (i.e. forming anthers in the female flower). Previous characterization indicated that the d1 mutation blocked three steps in GA biosynthesis; however, the locus has not been isolated and characterized. Here, we report that D1 encodes a GA 3-oxidase catalyzing the final step of bioactive GA synthesis. Recombinant D1 is capable of converting GA 20 to GA 1 , GA 20 to GA 3 , GA 5 to GA 3 , and GA 9 to GA 4 in vitro. These reactions are widely believed to take place in the cytosol. However, both in vivo GFP fusion analysis and westernblot analysis of organelle fractions using a D1-specific antibody revealed that the D1 protein is dual localized in the nucleus and cytosol. Furthermore, the upstream gibberellin 20-oxidase1 (ZmGA20ox1) protein was found dual localized in the nucleus and cytosol as well. These results indicate that bioactive GA can be synthesized in the cytosol and the nucleus, two compartments where GA receptor Gibberellin-insensitive dwarf protein1 exists. Furthermore, the D1 protein was found to be specifically expressed in the stamen primordia in the female floret, suggesting that the suppression of stamen development is mediated by locally synthesized GAs.

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