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To the editor Coronavirus disease 2019 (COVID-19), which emerged in Wuhan, China in December 2019, is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has become a major global public health concern [1]. Positive detection of SARS-CoV-2 RNA in nasopharyngeal swab samples, sputum samples or bronchoalveolar lavage samples by reverse transcriptase polymerase chain reaction (RT-PCR) has been used to confirm SARS-CoV-2 infection [2]. Recently, positive detection of IgM and IgG antibodies specific to SARS-CoV-2 has also been recognized as deterministic evidence for confirmed SARS-CoV-2 infection [3,4]. However, the antibody response to SARS-CoV-2 currently remains inadequately understood in COVID-19 patients. In the present study, we investigated the patterns of antibody response to SARS-CoV-2 in patients with COVID-19, aiming to better clarify the humoral immunological response during SARS-CoV-2 infection.

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Ly-6A is a murine antigen which is implicated in lymphocyte activation and may be involved in activation of hematopoietic stem cells. Antibody cross-linking studies and antisense experiments have suggested that Ly-6A is a lymphocyte coactivation molecule. To better understand the function of Ly-6A, we used gene targeting to produce Ly-6A null mice which are healthy and have normal numbers and percentages of hematopoietic lineages. However, T lymphocytes from Ly-6A–deficient animals proliferate at a significantly higher rate in response to antigens and mitogens than wild-type littermates. In addition, Ly-6A mutant splenocytes generate more cytotoxic T lymphocytes compared to wild-type splenocytes when cocultured with alloantigen. This enhanced proliferation is not due to alterations in kinetics of response, sensitivity to stimulant concentration, or cytokine production by the T cell population, and is manifest in both in vivo and in vitro T cell responses. Moreover, T cells from Ly-6A–deficient animals exhibit a prolonged proliferative response to antigen stimulation, thereby suggesting that Ly-6A acts to downmodulate lymphocyte responses.

Liu X, He L, Stensaas L, Dinger B, Fidone S. Adaptation to chronic hypoxia involves immune cell invasion and increased expression of inflammatory cytokines in rat carotid body. Am J Physiol Lung Cell Mol Physiol 296: L158 -L166, 2009. First published October 31, 2008 doi:10.1152/ajplung.90383.2008.-Exposure to chronic hypoxia (CH; 3-28 days at 380 Torr) induces adaptation in mammalian carotid body such that following CH an acute hypoxic challenge elicits an abnormally large increase in carotid sinus nerve impulse activity. The current study examines the hypothesis that CH initiates an immune response in the carotid body and that chemoreceptor hyperexcitability is dependent on the expression and action of inflammatory cytokines. CH resulted in a robust invasion of ED1 ϩ macrophages, which peaked on day 3 of exposure. Gene expression of proinflammatory cytokines, IL-1␤, TNF␣, and the chemokine, monocyte chemoattractant protein-1, was increased Ͼ2-fold after 1 day of hypoxia followed by a Ͼ2-fold increase in IL-6 on day 3. After 28 days of CH, IL-6 remained elevated Ͼ5-fold, whereas expression of other cytokines recovered to normal levels. Cytokine expression was not restricted to immune cells. Studies of cultured type I cells harvested following 1 day of in vivo hypoxia showed elevated transcript levels of inflammatory cytokines. In situ hybridization studies confirmed expression of IL-6 in type I cells and also showed that CH induces IL-6 expression in supporting type II cells. Concurrent treatment of CH rats with anti-inflammatory drugs (ibuprofen or dexamethasone) blocked immune cell invasion and severely reduced CH-induced cytokine expression in carotid body. Drug treatment also blocked the development of chemoreceptor hypersensitivity in CH animals. Our findings indicate that chemoreceptor adaptation involves novel neuroimmune mechanisms, which may alter the functional phenotypes of type I cells and chemoafferent neurons. dexamethasone; interleukin-1␤; interleukin-6; tumor necrosis factor-␣ THE MAMMALIAN CAROTID BODY consists of integrated units of chemoreceptor, neural, glial, and vascular cells surrounded by connective tissue, which collectively constitute a highly adaptive chemosensory organ. Stimulus transduction occurs in paracrine type I (chemoreceptor) cells, which release multiple neuroactive agents in response to hypoxia, hypercapnia, and acidosis. Primary afferent neurons in the petrosal ganglia project axons through the carotid sinus nerve (CSN) to form synaptic terminals on type I cells, whereas glial-like type II cells envelop the type I cells and terminal axon enlargements, forming lobules that are embedded in connective tissue penetrated by a microvascular network of highly permeable sinusoidal capillaries. Fibroblasts, resident macrophages, and a small number of mast cells are also present in the tissue together with postganglionic parasympathetic and sympathetic axons (24).Prolonged and continuous exposure of mammals to a low PO 2 environment (i.e., chronic hypoxia; CH) elicits adaptation in...

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2,4-Dichlorophenoxyacetic acid is a selective systemic herbicide for the control of broad-leaved weeds, which is widely used throughout the world. The persistence of its residues and its potential to migrate in the soil make it necessary to reduce its concentrations in contaminated soil and groundwater. The nature of this compound makes it particularly toxic to the broad-leaved plants, such as the poplar (Populus) and willow (Salix), which are often used in phytoremediation projects. We describe the inoculation of a model plant, the pea (Pisum sativum), with a genetically tagged bacterial endophyte that naturally possesses the ability to degrade 2,4-dichlorophenoxyacetic acid. The results showed that this strain actively colonized inoculated plants internally (and in the rhizosphere). Inoculated plants showed a higher capacity for 2,4-dichlorophenoxyacetic acid removal from soil and showed no 2,4-dichlorophenoxyacetic acid accumulation in their aerial tissues. This demonstrates the usefulness of bacterial endophytes to enhance the phytoremediation of herbicide-contaminated substrates and reduce levels of toxic herbicide residues in crop plants.

The deuterium excess is a second-order parameter linking water-stable oxygen and hydrogen isotopes and has been widely used in hydrological studies. The deuterium excess in precipitation is greatly influenced by below-cloud evaporation through unsaturated air, especially in an arid climate. Based on an observation network of isotopes in precipitation of arid central Asia, the difference in deuterium excess from cloud base to ground was calculated for each sampling site. The difference on the southern slope of the Tian Shan is generally larger than that on the northern slope, and the difference during the summer months is greater than that during the winter months. Generally, an increase of 1% in evaporation of raindrops causes deuterium excess to decrease by approximately 1‰. Under conditions of low air temperature, high relative humidity, heavy precipitation, and large raindrop diameter, a good linear correlation is exhibited between evaporation proportion and difference in deuterium excess, and a linear regression slope of <1‰ %−1 can be seen; in contrast, under conditions of high air temperature, low relative humidity, light precipitation, and small raindrop diameter, the linear relationship is relatively weak, and the slope is much larger than 1‰ %−1. A sensitivity analysis under different climate scenarios indicates that, if air temperature has increased by 5°C, deuterium excess difference decreases by 0.3‰–4.0‰ for each site; if relative humidity increases by 10%, deuterium excess difference increases by 1.1‰–10.3‰.