Abstract:Objectives
. Antiviral adaptive immunity involves memory B-(MBC) and T-cells (MTC), however their dynamics in SARS-CoV-2 convalescents warrant further investigation.
Methods
. In the cross-sectional and longitudinal study, we evaluated blood-derived MBC- and MTC-responses in 68 anti-spike IgG-positive mild-COVID-19 convalescents at visit 1 between 1-7 months (median 4.1 months) after disease onset. SARS-CoV-2 anti-spike IgG was performed by ELISA, MBC by SARS-COV-2 spec… Show more
“…et al ( 226 ) detected memory T cells, which secrete IFN-γ and are able to clonally expand following SARS-CoV-2-antigen re-exposure, at least three months after disease onset. Further investigations have detected maintained SARS-CoV-2-specific memory T cell responses in COVID-19 convalescent patients at least 7-12 months after infection ( 217 , 221 , 227 ) and this has been found to be true regardless of disease severity ( 227 ). Considering immune memory at the tissue level, SARS-CoV-2-specific lung resident memory T cell can be detected at least 10 months following infection ( 228 ).…”
Section: Immune Memorymentioning
confidence: 95%
“…et al (245) defined most SARS-CoV-2 CD4+ T cells as displaying a central memory profile. Furthermore, Gurevich M. et al (221) reported the presence of IL-2-secreting and IFN-g+IL-2-secreting SARS-CoV-2-specific central memory T cells that might be long-lasting memory phenotypes in accordance with previous studies (246). There are two different subsets of CCR7+ stem cell-like progenitors: CCR7+PD-1−TIGIT− cells are observed to display stem cell-like features, whereas CCR7+PD-1+TIGIT+ cells seem to exhibit exhausted traits (192,247).…”
Section: Immune Memory Phenotypesmentioning
confidence: 99%
“…There are some studies that report relatively stable humoral immunity for up to 6-12 moths post-infection ( 217 – 221 ) and Zhang J. et al ( 217 ) described the detection of neutralizing antibodies in convalescent COVID-19 patients even at 12 months following symptoms onset. However, further studies show a clear decline of SARS-CoV-2 neutralizing antibodies in the first months after infection ( 222 – 224 ), along with a progressive decline in total antibody levels eight months after SARS-CoV-2 infection ( 218 , 225 ).…”
Two years after the appearance of the SARS-CoV-2 virus, the causal agent of the current global pandemic, it is time to analyze the evolution of the immune protection that infection and vaccination provide. Cellular immunity plays an important role in limiting disease severity and the resolution of infection. The early appearance, breadth and magnitude of SARS-CoV-2 specific T cell response has been correlated with disease severity and it has been thought that T cell responses may be sufficient to clear infection with minimal disease in COVID-19 patients with X-linked or autosomal recessive agammaglobulinemia. However, our knowledge of the phenotypic and functional diversity of CD8+ cytotoxic lymphocytes, CD4+ T helper cells, mucosal-associated invariant T (MAIT) cells and CD4+ T follicular helper (Tfh), which play a critical role in infection control as well as long-term protection, is still evolving. It has been described how CD8+ cytotoxic lymphocytes interrupt viral replication by secreting antiviral cytokines (IFN-γ and TNF-α) and directly killing infected cells, negatively correlating with stages of disease progression. In addition, CD4+ T helper cells have been reported to be key pieces, leading, coordinating and ultimately regulating antiviral immunity. For instance, in some more severe COVID-19 cases a dysregulated CD4+ T cell signature may contribute to the greater production of pro-inflammatory cytokines responsible for pathogenic inflammation. Here we discuss how cellular immunity is the axis around which the rest of the immune system components revolve, since it orchestrates and leads antiviral response by regulating the inflammatory cascade and, as a consequence, the innate immune system, as well as promoting a correct humoral response through CD4+ Tfh cells. This review also analyses the critical role of cellular immunity in modulating the development of high-affinity neutralizing antibodies and germinal center B cell differentiation in memory and long-lived antibody secreting cells. Finally, since there is currently a high percentage of vaccinated population and, in some cases, vaccine booster doses are even being administered in certain countries, we have also summarized newer approaches to long-lasting protective immunity and the cross-protection of cellular immune response against SARS-CoV-2.
“…et al ( 226 ) detected memory T cells, which secrete IFN-γ and are able to clonally expand following SARS-CoV-2-antigen re-exposure, at least three months after disease onset. Further investigations have detected maintained SARS-CoV-2-specific memory T cell responses in COVID-19 convalescent patients at least 7-12 months after infection ( 217 , 221 , 227 ) and this has been found to be true regardless of disease severity ( 227 ). Considering immune memory at the tissue level, SARS-CoV-2-specific lung resident memory T cell can be detected at least 10 months following infection ( 228 ).…”
Section: Immune Memorymentioning
confidence: 95%
“…et al (245) defined most SARS-CoV-2 CD4+ T cells as displaying a central memory profile. Furthermore, Gurevich M. et al (221) reported the presence of IL-2-secreting and IFN-g+IL-2-secreting SARS-CoV-2-specific central memory T cells that might be long-lasting memory phenotypes in accordance with previous studies (246). There are two different subsets of CCR7+ stem cell-like progenitors: CCR7+PD-1−TIGIT− cells are observed to display stem cell-like features, whereas CCR7+PD-1+TIGIT+ cells seem to exhibit exhausted traits (192,247).…”
Section: Immune Memory Phenotypesmentioning
confidence: 99%
“…There are some studies that report relatively stable humoral immunity for up to 6-12 moths post-infection ( 217 – 221 ) and Zhang J. et al ( 217 ) described the detection of neutralizing antibodies in convalescent COVID-19 patients even at 12 months following symptoms onset. However, further studies show a clear decline of SARS-CoV-2 neutralizing antibodies in the first months after infection ( 222 – 224 ), along with a progressive decline in total antibody levels eight months after SARS-CoV-2 infection ( 218 , 225 ).…”
Two years after the appearance of the SARS-CoV-2 virus, the causal agent of the current global pandemic, it is time to analyze the evolution of the immune protection that infection and vaccination provide. Cellular immunity plays an important role in limiting disease severity and the resolution of infection. The early appearance, breadth and magnitude of SARS-CoV-2 specific T cell response has been correlated with disease severity and it has been thought that T cell responses may be sufficient to clear infection with minimal disease in COVID-19 patients with X-linked or autosomal recessive agammaglobulinemia. However, our knowledge of the phenotypic and functional diversity of CD8+ cytotoxic lymphocytes, CD4+ T helper cells, mucosal-associated invariant T (MAIT) cells and CD4+ T follicular helper (Tfh), which play a critical role in infection control as well as long-term protection, is still evolving. It has been described how CD8+ cytotoxic lymphocytes interrupt viral replication by secreting antiviral cytokines (IFN-γ and TNF-α) and directly killing infected cells, negatively correlating with stages of disease progression. In addition, CD4+ T helper cells have been reported to be key pieces, leading, coordinating and ultimately regulating antiviral immunity. For instance, in some more severe COVID-19 cases a dysregulated CD4+ T cell signature may contribute to the greater production of pro-inflammatory cytokines responsible for pathogenic inflammation. Here we discuss how cellular immunity is the axis around which the rest of the immune system components revolve, since it orchestrates and leads antiviral response by regulating the inflammatory cascade and, as a consequence, the innate immune system, as well as promoting a correct humoral response through CD4+ Tfh cells. This review also analyses the critical role of cellular immunity in modulating the development of high-affinity neutralizing antibodies and germinal center B cell differentiation in memory and long-lived antibody secreting cells. Finally, since there is currently a high percentage of vaccinated population and, in some cases, vaccine booster doses are even being administered in certain countries, we have also summarized newer approaches to long-lasting protective immunity and the cross-protection of cellular immune response against SARS-CoV-2.
“…In mild COVID-19 convalescents, the peak memory B cell response was detected at 3 months after symptom onset and persisted up to 7 months after infection. Significant memory T cell levels were detected 1 month after disease onset and persisted even when specific humoral immunity declined [ 79 ]. The level of immune responses at 1 year post-COVID-19, mainly the phagocytic capacity and memory B cell responses, depended on the severity of the prior COVID-19 [ 80 ].…”
Section: Immune Response To Sars-cov-2 Infectionmentioning
The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is associated with a robust immune response. The development of systemic inflammation leads to a hyperinflammatory state due to cytokine release syndrome during severe COVID-19. The emergence of many new SARS-CoV-2 variants across the world deteriorates the protective antiviral immunity induced after infection or vaccination. The innate immune response to SARS-CoV-2 is crucial for determining the fate of COVID-19 symptomatology. T cell-mediated immunity is the main factor of the antiviral immune response; moreover, SARS-CoV-2 infection initiates a rapid B-cell response. In this paper, we present the current state of knowledge on immunity after COVID-19 infection and vaccination. We discuss the mechanisms of immune response to various types of vaccines (nucleoside-modified, adenovirus-vectored, inactivated virus vaccines and recombinant protein adjuvanted formulations). This includes specific aspects of vaccination in selected patient populations with altered immune activity (the elderly, children, pregnant women, solid organ transplant recipients, patients with systemic rheumatic diseases or malignancies). We also present diagnostic and research tools available to study the anti-SARS-CoV-2 cellular and humoral immune responses.
“…IgM peaks on day 11-13 then decrease after 3 weeks besides IgG will be observed entirely on day 17-19 ( 52 ). The increase in IgG is followed by the formation of memory B cells for up to 3 months in length ( 53 ). Nevertheless, some patients with mild or asymptomatic symptoms were not found to be any seroconversion of these antibodies ( 54 ).…”
Section: Specific Immunity Against Sars-cov-2mentioning
Finding a vaccine that can last a long time and effective against viruses with high mutation rates such as SARS-CoV-2 is still a challenge today. The various vaccines that have been available have decreased in effectiveness and require booster administration. As the professional antigen presenting cell, Dendritic Cells can also activate the immune system, especially T cells. This ability makes dendritic cells have been developed as vaccines for some types of diseases. In SARS-CoV-2 infection, T cells play a vital role in eliminating the virus, and their presence can be detected in the long term. Hence, this condition shows that the formation of T cell immunity is essential to prevent and control the course of the disease. The construction of vaccines oriented to induce strong T cells response can be formed by utilizing dendritic cells. In this article, we discuss and illustrate the role of dendritic cells and T cells in the pathogenesis of SARS-CoV-2 infection and summarizing the crucial role of dendritic cells in the formation of T cell immunity. We arrange the basis concept of developing dendritic cells for SARS-CoV-2 vaccines. A dendritic cell-based vaccine for SARS-CoV-2 has the potential to be an effective vaccine that solves existing problems.
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