Ability of the immune system to fight viruses highlighted by cytometry and T-cell receptor clonotype assessment: lessons taken before the coronavirus disease 2019 pandemic outbreak.

The intriguing aspects of severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2) are the high rate of spread and rapid progression of pneumonitis. Confronted with thousands of deaths daily worldwide, we have to quickly build the rationale behind the treatment, taking advantage of past analogues. When a new virus strikes, T‑cell receptor γδ cells are in the first line of defense, activated by stress molecules and recognizing some epitopes in a process that is major histocompatibility complex-independent but still specific, eg, cytomegalovirus, as well as participating in the regulatory mechanism-both characteristics are useful in fighting SARS‑CoV‑2. Most deaths occur due to pneumonitis, in the course of which overwhelming inflammation impairs blood oxygenation, calling for artificial ventilation. In fatal cases of coronavirus disease 2019, the balance between the immune response and the inflammatory outcome fails and, therefore, patients at risk, mostly the elderly, show higher levels of anti-SARS‑CoV‑2 antibodies and enhanced inflammation in the lungs. Apparently, there is no feedback control over the antibody production. The investigational use of convalescent plasma, providing antibodies taken from patients who have recovered, was shown to be effective, likely through exerting idiotype‑associated negative control of antibody production. Similarly, the use of mesenchymal stem cells may assist the body regulatory mechanisms, considering the anti‑inflammatory potential of these cells. The use of these 2 immunotherapeutic tools is understandable based on basic immunology and this knowledge may direct the efforts of the medical community aimed at combating the virus.