Corpus overview


MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

There are no SARS-CoV-2 protein terms in the subcorpus


SARS-CoV-2 Proteins
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    Blocking of the CD80 HGNC/86 axis as a therapeutic approach to prevent progression to more severe forms of COVID-19 MESHD

    Authors: Antonio Julià; Irene Bonafonte; Antonio Gómez; María López-Lasanta; Mireia López-Corbeto; Sergio H. Martínez-Mateu; Jordi Lladós; Iván Rodríguez-Nunez; Richard M. Myers; Sara Marsal

    id:2005.10055v1 Date: 2020-05-20 Source: arXiv

    In its more severe forms, COVID-19 MESHD progresses towards an excessive immune response, leading to the systemic overexpression of proinflammatory cytokines like IL6 HGNC, mostly from the infected lungs MESHD. This cytokine storm can cause multiple organ damage and death. Consequently, there is a pressing need to identify therapies to treat and prevent severe symptoms during COVID-19 MESHD. Based on previous clinical evidence, we hypothesized that inhibiting T cell co-stimulation by blocking CD80 HGNC/86 could be an effective therapeutic strategy against progression to severe proinflammatory states. To support this hypothesis, we performed an analysis integrating blood transcriptional data we generated from rheumatoid arthritis MESHD patients treated with abatacept -- a CD80 HGNC/86 co-stimulation inhibitor -- with the pathological features associated with COVID-19 MESHD, particularly in its more severe forms. We have found that many of the biological processes that have been consistently associated with COVID-19 MESHD pathology are reversed by CD80 HGNC/86 co-stimulation inhibition, including the downregulation of IL6 HGNC production. Also, analysis of previous transcriptional data from blood of SARS-CoV-infected MESHD patients showed that the response to abatacept has a very high level of antagonism to that elicited by COVID-19 MESHD. Finally, analyzing a recent single cell RNA-seq dataset from bronchoalveolar lavage fluid cells from COVID-19 MESHD patients, we found a significant correlation along the main elements of the C80/86 axis: CD86 HGNC+/80+ antigen presenting cells, activated CD4+ T cells and IL6 HGNC production. Our in-silico study provides additional support to the hypothesis that blocking of the CD80 HGNC/ CD86 HGNC signaling axis may be protective of the excessive proinflammatory state associated with COVID-19 MESHD in the lungs.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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