Notes

Hydroxychloroquine as well as COVID-19: could we learn from the usage of rituximab throughout endemic lupus erythematosus?
Naive CD4+ T cells become memory cells after proliferating in response to their cognate major histocompatibility complex class II (MHCII)-bound peptide and passing through an effector cell stage. The process by which CD4+ memory T cells emerge from the effector cell pool, however, is less well understood than in the case of CD8+ T cells. During certain acute infections, naive CD4+ T cells proliferate and differentiate into various forms of type 1 (Th1) and follicular helper (Tfh) effector cells. We review the evidence that about 10% of the cells in each of these subsets survive to become memory cells that resemble their effector cell precursors. The roles that asymmetric cell division, the TCF-1 transcription factor, metabolic activity, reactive oxygen species, and the IL-7 receptor play in the effector to memory cell transition are discussed. We propose a speculative model in which the metabolic activity needed for rapid clonal expansion also generates toxic products that induce apoptosis in most effector cells. Memory cells then arise from the effector cells in each subset that are at the low end of the metabolic activity spectrum.Auxin is a crucial growth regulator that governs plant development and responses to environmental perturbations. It functions at the heart of many developmental processes, from embryogenesis to organ senescence, and is key to plant interactions with the environment, including responses to biotic and abiotic stimuli. As remarkable as auxin is, it does not act alone, but rather solicits the help of, or is solicited by, other endogenous signals, including the plant hormones abscisic acid, brassinosteroids, cytokinins, ethylene, gibberellic acid, jasmonates, salicylic acid, and strigolactones. The interactions between auxin and other hormones occur at multiple levels hormones regulate one another's synthesis, transport, and/or response; hormone-specific transcriptional regulators for different pathways physically interact and/or converge on common target genes; etc. However, our understanding of this crosstalk is still fragmentary, with only a few pieces of the gigantic puzzle firmly established. In this review, we provide a glimpse into the complexity of hormone interactions that involve auxin, underscoring how patchy our current understanding is.Plants, in contrast to animals, are unique in their capacity to postembryonically develop new organs due to the activity of stem cell populations, located in specialized tissues called meristems. Above ground, the shoot apical meristem generates aerial organs and tissues throughout plant life. It is well established that auxin plays a central role in the functioning of the shoot apical meristem. Auxin distribution in the meristem is not uniform and depends on the interplay between biosynthesis, transport, and degradation. Auxin maxima and minima are created, and result in transcriptional outputs that drive the development of new organs and contribute to meristem maintenance. To uncover and understand complex signaling networks such as the one regulating auxin responses in the shoot apical meristem remains a challenge. Here, we will discuss our current understanding and point to important research directions for the future.The molecular basis of the persistence of experienced T lymphocytes, also known as "memory T lymphocytes," is still enigmatic. We are beginning to understand their considerable heterogeneity and topographic compartmentalization into memory T cells circulating through the body and those residing in a particular tissue. In some tissues, like murine spleen, subpopulations of memory T cells proliferating in the absence of antigen (homeostatic proliferation) have been described. Other populations are maintained resting in terms of transcription, mobility, and proliferation in dedicated survival niches organized by stromal cells. The survival of these memory T cells is conditional on being in such a niche, where they can persist for a lifetime. Circulating memory T lymphocytes of distinct immune responses slowly decline in numbers over time. The rules governing their entry into and exit from blood, as well as their lifestyle outside of the blood and their relation to resident memory T cells are poorly understood. Homeostasis of circulating, proliferating, and resting memory T cells is obviously controlled by different rheostats tissue-exit and tissue-entry signals for circulating and proliferation-inducing signals for proliferating memory T cells. For tissue-resident, resting memory T cells, it is the availability of their survival niche. Selleck VBIT-4 Apparently, this mechanism (i.e., the link between memory T cell and stromal cell) is so robust that it provides efficient T-cell memory over a lifetime in tissues such as the bone marrow.The auxin-binding protein 1 (ABP1) has endured a history of undulating prominence as a candidate receptor for this important phytohormone. Its capacity for binding auxin has not been in doubt, a feature adequately explained by its crystal structure, but any relevance of this to auxin signaling and plant development has been far more demanding to define. Over its research lifetime, it has been associated with many auxin-induced activities, including ion fluxes across the plasma membrane, rearrangement of the cytoskeleton and cell shape, and the abundance of PIN proteins at the plasma membrane via control of endocytosis, all of which required its presence in the apoplast. Yet, ABP1 has a KDEL sequence that targets it to the endoplasmic reticulum, where most of it remains. This mismatch has been more than adequately compensated for by the need for an auxin receptor to account for responses far too rapid to be executed through transcription and translation and the TIR1/AuxIAA coreceptor system. However, discoveries showing that abp1-null mutants are not compromised for auxin signaling or development, that TIR1 or AFB1 are necessarily involved with very rapid responses at the plasma membrane, and that these rapid responses are mediated with intracellular auxin all suggest that ABP1's auxin-binding capacity is not physiologically relevant. Nevertheless, ABP1 is ubiquitous in higher plants and throughout plant tissues. We need to complete its history by defining its function inside plant cells.
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