Human T lymphocyte. (
Photo: NASA’s Marshall Space Flight Center / Flickr.com)-
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Speaking of acquired immunity, we usually mean antibodies (immunoglobulins) and B cells that produce them. B-cells shuffle DNA fragments that encode antibodies, and as a result of such shuffling, we can get antibodies to almost any pathogen. During a viral infection, among many B cells, an advantage is given to those that synthesize antibodies to the proteins of the virus that we have infected – such B cells turn into so-called plasmocytes that synthesize antibodies, as they say, on an industrial scale. In addition, some of the B cells become memory B cells – since they can produce antibodies against a specific virus, the immune system saves them in case the virus reappears.
But acquired immunity is not only B cells. There are also T cells that stimulate B cells to work more energetically against a pathogen, helping them to recognize molecules that belong to the pathogen (the so-called T-helpers). Other T cells – T-killers – destroy infected cells along with the infection that multiplies in them. Infected cells expose fragments of viral proteins on their surface (if we are talking about a viral infection), and T-killers specifically respond to these viral proteins.
The reaction of T-lymphocytes can be strong or weak, and in the case of the new SARS-CoV-2 coronavirus, it was still not clear whether T-cells respond to it at all. This was decided to check the researchers from the Institute of Immunology in La Jolla and other research centers. First, they analyzed the proteins of the virus for what pieces of viral proteins could cause the strongest T-lymphocyte response, and then they took the protein fragments thus selected and added them to the T-lymphocytes taken from ten patients who had a mild coronavirus infection COVID-19.
In article in Cell it is said that all patients had T-helpers recognizing coronavirus protein S – the very one by which the virus penetrates the cell. If T-helpers recognize this protein, they will be able to boost the activity of those B cells that are ready to synthesize antibodies against it. In addition, among the T-helpers were those that recognized other SARS-CoV-2 proteins.
As for T-killers that respond precisely to SARS-CoV-2 infection, they were found in 70% of the participants in the experiment. That is, we can say that the T-cell part of the acquired immunity quite sees the coronavirus and is involved in the fight against it. And perhaps this should be considered when developing vaccines for coronavirus. (Now, as the portal writes ScienceSARS-CoV-2 vaccines are being developed over a hundred.)
But the most interesting was discovered when T cells targeting the new coronavirus tried to search for those who had never infected SARS-CoV-2. Nearly seventy of these people were involved in the study, and 34% had T-helper lymphocytes that recognized the new coronavirus – although, we repeat, these people never infected them, and half of the blood samples were anti-SARS-CoV-2 with T cells generally referred to 2015–2018, when no one even heard of SARS-CoV-2.
Most likely, other coronaviruses helped here: as you know (and as we wrote in one of our articles), among human coronaviruses there are those that cause nothing more serious than colds. Moreover, the proteins of the “cold” coronaviruses are somewhat similar to the proteins of their more serious counterparts, including the SARS-CoV-2 proteins. Therefore, as the authors of the work believe, immune cells that have learned to recognize old and familiar coronaviruses may well respond to the new coronavirus. This gives hope that a new coronavirus infection will not be able to go beyond any limits – after all, old coronaviruses are quite common among people, and therefore a new infection for immunity is often not so new.
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