The UV upturn phenomenon in elliptical galaxies, although challenging because of its complexity, is attractive for its potential value as an age indicator of old stellar systems. This work represents the combined efforts of two population synthesis groups with substantially different views to work together to minimize uncertainties in modeling and analysis. Unfortunately, this study, using the currently available data, cannot determine the metallicity of the dominant UV sources, one of the most outstanding problems related to the UV upturn phenomenon, as some input parameters need to be constrained better. We have found, however, that it is feasible to select a more likely model empirically because different models predict substantially different UV-to-V flux ratios as functions of redshift: metal-rich solutions predict a much steeper decline in the UV-to-V flux ratio than metal-poor solutions. We show that such differences in model predictions are quite independent of cosmology and are detectable using current and upcoming space UV facilities.The various alternatives suggest significantly different ages for the present epoch giant ellipticals: the metal-rich solutions suggest 30 -50% smaller ages than the metal-poor solutions. Thus, an empirical fitting would not only reveal the origin of the UV upturn but yield independent age estimations for ellipticals.We show that this may effectively constrain some of the cosmological parameters that predict a unique age for the present epoch galaxies. If we use the most recent estimations of H 0 and Ω 0 , the younger, metal-rich models would have no conflict with a cosmology of a negligibly small Λ 0 , while the older, metal-poor models unavoidably suggest a substantially large value of Λ 0 (i.e., Λ 0 ∼ > 0.63 for z f or = ∞) in the context of an inflationary universe.-3 -

T cells of the γδ lineage are unconventional T cells with functions not restricted to MHC-mediated antigen presentation. Because of their broad antigen specificity and NK-like cytotoxicity, γδ T-cell importance in tumor immunology has been emphasized. However, some γδ T-cell subsets, especially those expressing IL-17, are immunosuppressive or tumor-promoting cells. Their cytokine profile and cytotoxicity are seemingly determined by cross-talk with microenvironment components, not by the γδTCR chain. Furthermore, much about the TCR antigen of γδ T cells remains unknown compared with the extreme diversity of their TCR chain pairs. Thus, the investigation and application of γδ T cells have been relatively difficult. Nevertheless, γδ T cells remain attractive targets for antitumor therapy because of their independence from MHC molecules. Because tumor cells have the ability to evade the immune system through MHC shedding, heterogeneous antigens, and low antigen spreading, MHC-independent γδ T cells represent good alternative targets for immunotherapy. Therefore, many approaches to using γδ T cells for antitumor therapy have been attempted, including induction of endogenous γδ T cell activation, adoptive transfer of expanded cells ex vivo, and utilization of chimeric antigen receptor (CAR)-T cells. Here, we discuss the function of γδ T cells in tumor immunology and their application to cancer therapy.

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SARS-CoV-2 infection has recently been declared a pandemic. Some patients showing severe symptoms exhibit drastic inflammation and airway damage. In this study, we re-analyzed published scRNA-seq data of COVID-19 patient bronchoalveolar lavage fluid to further classify and compare immunological features according to the patient’s disease severity. Patients with severe symptoms showed DNA damage and apoptotic features of epithelial cells. Our results suggested that epithelial damage was associated with neutrophil infiltration. Myeloid cells of severe patients showed higher expression of proinflammatory cytokines and chemokines such as CXCL8. As a result, neutrophils were abundant in lungs of patients from the severe group. Furthermore, recruited neutrophils highly expressed genes related to neutrophil extracellular traps. Neutrophil-mediated inflammation was regulated by glucocorticoid receptor expression and activity. Based on these results, we suggest that severe COVID-19 symptoms may be determined by differential expression of glucocorticoid receptors and neutrophils.

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