Cellular and Humoral Immune Responses in Covid-19 and Immunotherapeutic Approaches

被引:40
作者
Hasan, Amal [1 ]
Al-Ozairi, Ebaa [2 ,3 ]
Al-Baqsumi, Zahraa [1 ]
Ahmad, Rasheed [1 ]
Al-Mulla, Fahd [4 ]
机构
[1] Dasman Diabet Inst, Dept Immunol & Microbiol, Res Div, Kuwait, Kuwait
[2] Dasman Diabet Inst, Med Div, Clin Res Unit, Kuwait, Kuwait
[3] Fac Med, Dept Med, Kuwait, Kuwait
[4] Dasman Diabet Inst, Dept Genet & Bioinformat, Res Div, Funct Genom, Kuwait, Kuwait
关键词
SARS-CoV-2; inflammation; immune regulation; neutralizing antibodies; cytokines; autoantibodies; type I interferon; ACUTE-RESPIRATORY-SYNDROME; CORONAVIRUS SARS-COV; NEUTROPHIL EXTRACELLULAR TRAPS; ANTIBODY-DEPENDENT ENHANCEMENT; RECEPTOR-BINDING DOMAIN; CONVERTING ENZYME 2; CD4(+) T-CELLS; CONVALESCENT PLASMA; SPIKE PROTEIN; MERS-COV;
D O I
10.2147/ITT.S280706
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Coronavirus disease 2019 (Covid-19), caused by the novel coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), can range in severity from asymptomatic to severe/critical disease. SARS-CoV-2 uses angiotensin-converting enzyme 2 to infect cells leading to a strong inflammatory response, which is most profound in patients who progress to severe Covid-19. Recent studies have begun to unravel some of the differences in the innate and adaptive immune response to SARS-CoV-2 in patients with different degrees of disease severity. These studies have attributed the severe form of Covid-19 to a dysfunctional innate immune response, such as a delayed and/or deficient type I interferon response, coupled with an exaggerated and/or a dysfunctional adaptive immunity. Differences in T-cell (including CD4(+) T-cells, CD8(+) T-cells, T follicular helper cells, gamma delta-T-cells, and regulatory T-cells) and B-cell (transitional cells, double-negative 2 cells, antibody-secreting cells) responses have been identified in patients with severe disease compared to mild cases. Moreover, differences in the kinetic/titer of neutralizing antibody responses have been described in severe disease, which may be confounded by antibody-dependent enhancement. Importantly, the presence of preexisting autoantibodies against type I interferon has been described as a major cause of severe/critical disease. Additionally, priorVaccine and multiple vaccine exposure, trained innate immunity, cross-reactive immunity, and serological immune imprinting may all contribute towards disease severity and outcome. Several therapeutic and preventative approaches have been under intense investigations; these include vaccines (three of which have passed Phase 3 clinical trials), therapeutic antibodies, and immunosuppressants.
引用
收藏
页码:63 / 85
页数:23
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