Fighting COVID-19 exhausts T cells

Moon, Chang Yoon

doi:10.1038/s41577-020-0304-7

Cited by 97 publications

(100 citation statements)

References 2 publications

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“…Consistent with previous work, these markers were significantly elevated in critically ill patients compared with those who were only mildly symptomatic with COVID-19 ( 46 ). This new data indicates that SARS-CoV-2 promotes extreme stimulation and ensuing exhaustive collapse of CD8 + T cells, which is similar in fashion to many malignancies ( 44 – 46 ).…”

Section: Immune Responsementioning

confidence: 55%

“…It was found that as patients progressed from prodromal to active symptoms, their levels of PD1 and Tim3 would directly increase. In the same vein, patients in the ICU had much higher expression of these markers compared to non-ICU and control populations ( 44 , 45 ). Another study used granzyme B and perforin markers of induced apoptosis as indicators of CD8+ cell fatigue.…”

Section: Immune Responsementioning

confidence: 80%

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What’s Sex Got to Do With COVID-19? Gender-Based Differences in the Host Immune Response to Coronaviruses

et al. 2020

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The novel severe acute respiratory syndrome coronavirus 2, the cause of the coronavirus disease 2019 (COVID-19) pandemic, has ravaged the world, with over 22 million total cases and over 770,000 deaths worldwide as of August 18, 2020. While the elderly are most severely affected, implicating an age bias, a striking factor in the demographics of this deadly disease is the gender bias, with higher numbers of cases, greater disease severity, and higher death rates among men than women across the lifespan. While pre-existing comorbidities and social, behavioral, and lifestyle factors contribute to this bias, biological factors underlying the host immune response may be crucial contributors. Women mount stronger immune responses to infections and vaccinations and outlive men. Sex-based biological factors underlying the immune response are therefore important determinants of susceptibility to infections, disease outcomes, and mortality. Despite this, gender is a profoundly understudied and often overlooked variable in research related to the immune response and infectious diseases, and it is largely ignored in drug and vaccine clinical trials. Understanding these factors will not only help better understand the pathogenesis of COVID-19, but it will also guide the design of effective therapies and vaccine strategies for gender-based personalized medicine. This review focuses on sex-based differences in genes, sex hormones, and the microbiome underlying the host immune response and their relevance to infections with a focus on coronaviruses.

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Section: Immune Responsementioning

confidence: 55%

Section: Immune Responsementioning

confidence: 80%

What’s Sex Got to Do With COVID-19? Gender-Based Differences in the Host Immune Response to Coronaviruses

et al. 2020

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“…In these patients, interleukin (IL)-6, IL-10, and tumor necrosis factor-alpha (TNFα) surge coincidental with peak adverse clinical symptoms, rapidly declining during recovery. Patients requiring intensive care unit admission have significantly higher levels of IL-6, IL-10, and TNFα and fewer T cells (12). This cytokine storm likely dampens innate adaptive immunity against SARS-CoV-2 infection.…”

Section: The Calm Before the Storm: Cytokine Storm Syndrome Lung Dammentioning

confidence: 99%

Does High Cardiorespiratory Fitness Confer Some Protection Against Proinflammatory Responses After Infection by SARS‐CoV‐2?

Zbinden‐Foncea

Francaux

Deldicque

et al. 2020

Obesity

166

144

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“…However, some authors highlighted the risk related to unbalanced use of immunosuppressive treatments, since failure of antiviral immunity to control SARS-CoV-2 replication could underlie the hyper-inflammatory responses characterizing severe COVID-19 [2]. In critically ill COVID-19 patients, indeed, massive cytokine storms (including IL-6, TNF-α, and other inflammatory biomarkers), as well as increments of circulating neutrophils and monocyte activation, are typically observed together with low T lymphocyte counts and functional exhaustion of effector T cell responses [1,3,4]. Such ineffective and detrimental expansions of innate/humoral responses, alongside T cell suppression, are reminiscent of classical features of sepsis, which is currently defined as a life-threatening organ dysfunction induced by dysregulated host response to infection, being characterized not only by systemic hyperinflammation (SIRS) with related endothelial and organ damage, but also by impairment of adaptive T cell immunity.…”

Section: Covid-19: Room For Treating T Cell Exhaustion?mentioning

confidence: 99%