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Using two independent single-cell approaches, we identified a shift in the overall immune cell composition in cavefish as the underlying cellular mechanism, indicating strong differences in the immune investment strategy. While surface fish invest evenly into the innate and adaptive immune systems, cavefish shifted immune investment to the adaptive immune system, and here, mainly towards specific T-cell populations that promote homeostasis. Additionally, inflammatory responses and immunopathological phenotypes in visceral adipose tissue are drastically reduced in cavefish. Our data indicate that long-term adaptation to low parasite diversity coincides with a more sensitive immune system in cavefish, which is accompanied by a reduction in the immune cells that play a role in mediating the pro-inflammatory response.

Among the many uncertainties that remain about Covid-19 is how the human immune system responds to infection and what that means for the spread of the disease. Immunity after any infection can range from lifelong and complete to nearly nonexistent. So far, however, only the first glimmers of data are available about immunity to SARS-CoV-2, the coronavirus that causes Covid-19.

The coronavirus disease 2019 (COVID-19) pandemic has underscored the critical need to better understand the human immune system and how to unleash its power to develop vaccines and therapeutics. Much of our knowledge of the immune system has accrued from studies in mice, yet vaccines and drugs that work effectively in mice do not always translate into humans. Pulendran and Davis review recent technological advances that have facilitated the study of the immune system in humans. They discuss new insights and how these can affect the development of drugs and vaccines in the modern era.

The differing immune system responses of patients with COVID-19 can help predict who will experience moderate and severe consequences of disease, according to a new study by Yale researchers published July 27 in the journal Nature.

we really need to understand how the immune system reacts to the coronavirus.

Now, a research group under the leadership of professor and virologist Søren Riis Paludan from the Department of Biomedicine at Aarhus University, Denmark, has identified a mechanism which is activated in the cells of the immune system when they are attacked by disease. The discovery involves the protein STING, which sends signals to the nucleus of the cell when an infection threatens.

At the beginning of the pandemic, the coronavirus looked to be another respiratory illness. But the virus has turned out to affect not just the lungs, but the kidneys, the heart and the circulatory system - even, somehow, our senses of smell and taste.

The virus flourishes by undermining the body's chemical defense system

More than a year after COVID-19 emerged, many mysteries persist about the disease: why do some people get so much sicker than others? Why does lung damage sometimes continue to worsen well after the body seems to have cleared the SARS-CoV-2 virus? And what is behind the extended, multi-organ illness that lasts for months in people with 'long COVID'? A growing number of studies suggest that some of these questions might be explained by the immune system mistakenly turning against the body - a phenomenon known as autoimmunity.