The extent of the immune response is correlated with prognosis to an extent.In thestageofa specific immune response, pulmonary endothelial cells produce a large volume of inflammatory factors are the first to increase, followed by IL and IL. IL is produced by stimulation caused by TNF and IL, and the peripheral blood concentration can be used to evaluate the intensity of the systemic inflammatory response. Early studies indicated that patients with COVID have high levels of exp ress ionof IL B, IFN, in terfe ron induced protein. In compar ison to patien ts with mild or moderate COVID not necess itating treatment in the ICU, patients with purchase Solvent Red 23 severe COVID in the ICU have higher serum levels of granulocyte colonystimulating factor as well as higher levels of expression of TNF, suggesting a correlation between the severity of disease and the occurrence of a cy tok inestorm. In addit ion, serum levels of IL, IL, and IL are also significantly elevated. An autopsy of patients with COVID revealed diffuse alveolar injury with fibrous mucusl ike exuda tes in bo th lungs, la rge numbe rsof shed cells and the fo rmationoftranspa rentmemb ranes, and inflamma to ry infilt rationof monocy tesin the alveolar stroma. In peripheral blood samples from patients who died of COVID, CD and CD T lymphocyte counts were decreased, human leukocyte antigen DR and the CD doublepositive T lymphocyte ratio significantly increased, implying that these immune T lymphocytes are excessively activated.After the seventh edition, immunotherapyhasbeenrec ommendedforthe management of severe and critical patients, tocilizumab is indicated for patients with severe disease, extensive lung in ju ry, andeleva ted IL levels acco rd ing to laboratory results. The following medications and therapies are listed to inhibit cytokine storms in patients with COVID: i G lucocortico ids. For crit icalcases or patien ts with immune activation, the benefits and risks should be promptly assessed, and caution should always be exercised regarding duration and dosage.Recent studies have found tocilizumab to be an effective therapeutic strategy, and especially in patients with severe COVID. By inhibiting the production and release of TNF and IL, these two drugs suppress the occurrence of a cytokine storm.Nearly clinical studies are currently examining different dosages of chloroquine, hydroxychloroquine, or both to treat COVID worldwide, and some of them actually involve severe and critical patients.Anticoagulation therapy protects endothelial cells and reduces cytokine release, alleviating the immune response.Currently, this compound hasp assedthemilestoneofph ase I, I I, and I I I clinical trials for five indications, including Targetmol’s Cuparene idiopathic pulmonary fibrosis and primary myelofibrosis.JAK transmits intracellular signals from cell surface receptors that act on various cytokines andgrow thfactorsin volv edininfl amm ati on and immune function, thus affecting the immune process.Different receptors can activate different subtypes of JAK, thus exhibiting differentiated biological functions. Earl iers tud iesfound thatinc rea sed levelsofpro inflamma to ry fac tors in plasma of SARS patients are associated with pneumonia and severe lung injury. JAK inhibitors can inhibit the JAKSTAT signaling pathway, reducing the level of IP express ion induced by S pro te in in mouse lungs and repairing the damage caused by a virus on the immune system.