T cell immunity to SARS-CoV-2

Nießl, Julia; Sekine, Takuya; Buggert, Marcus

doi:10.1016/j.smim.2021.101505

Cited by 63 publications

(59 citation statements)

References 125 publications

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“…This cross-reactivity may also explain the few HC who displayed high spike and nucleocapsid IgG titers. Both humoral and cellular immune responses that are cross-reactive with the common cold coronaviruses have been described, mostly within CD4 + T cells ( 33 ). Children have been previously infected with fewer coronaviruses than adults based upon years of life; however, endemic coronavirus infection in children may have been more recent, potentially accounting for the high T cell responses seen here in HC.…”

Section: Discussionmentioning

confidence: 99%

Limited induction of SARS-CoV-2–specific T cell responses in children with multisystem inflammatory syndrome compared with COVID-19

Singh¹,

Obregon-Perko²,

Lapp³

et al. 2022

JCI Insight

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Why Multisystem Inflammatory Syndrome in Children (MIS-C) develops after SARS-CoV-2 infection in a subset of children is unknown. We hypothesized that aberrant virusspecific T-cell responses contribute to MIS-C pathogenesis. We quantified SARS-CoV-2 reactive T-cells, serologic responses against major viral proteins, and cytokine responses from plasma and peripheral blood mononuclear cells in children with convalescent COVID-19, acute MIS-C, and healthy controls. Children with MIS-C had significantly lower virus-specific CD4+ and CD8+ T-cell responses to major SARS-CoV-2 antigens compared with children convalescing from COVID-19. Further, T-cell responses in participants with MIS-C were similar to or lower than those in healthy controls. Serologic responses against spike receptor binding domain (RBD), full-length spike, and nucleocapsid were similar among convalescent COVID-19 and MIS-C, suggesting functional B cell responses. Cytokine profiling demonstrated predominant Th1 polarization of CD4+ T-cells from children with convalescent COVID-19 and MIS-C, although cytokine production was reduced in MIS-C. Our findings support a role for constrained induction of anti-SARS-CoV-2-specific T-cells in the pathogenesis of MIS-C.

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Section: Discussionmentioning

confidence: 99%

Limited induction of SARS-CoV-2–specific T cell responses in children with multisystem inflammatory syndrome compared with COVID-19

Singh¹,

Obregon-Perko²,

Lapp³

et al. 2022

JCI Insight

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“…SARS-CoV-2-specific T cells have been identified in all T cell subsets, TCM, TEM, and TEMRA subsets in immunocompetent individuals. Indeed, several studies have demonstrated T cell memory and effector responses against a broad selection of epitopes from SARS-CoV-2, as well as cross-reactive responses in unexposed individuals ( 35 ). The majority of the immunocompetent subjects developed T-cell responses following immunization, with variable results observed only in aged individuals ( 36 ).…”

Section: Insight On Sars-cov-2mentioning

confidence: 99%

The Immune Response to SARS-CoV-2 Vaccination: Insights Learned From Adult Patients With Common Variable Immune Deficiency

2022

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CVID patients have an increased susceptibility to vaccine-preventable infections. The question on the potential benefits of immunization of CVID patients against SARS-CoV-2 offered the possibility to analyze the defective mechanisms of immune responses to a novel antigen. In CVID, as in immunocompetent subjects, the role of B and T cells is different between infected and vaccinated individuals. Upon vaccination, variable anti-Spike IgG responses have been found in different CVID cohorts. Immunization with two doses of mRNA vaccine did not generate Spike-specific classical memory B cells (MBCs) but atypical memory B cells (ATM) with low binding capacity to Spike protein. Spike-specific T-cells responses were also induced in CVID patients with a variable frequency, differently from specific T cells produced after multiple exposures to viral antigens following influenza virus immunization and infection. The immune response elicited by SARS-CoV-2 infection was enhanced by subsequent immunization underlying the need to immunize convalescent COVID-19 CVID patients after recovery. In particular, immunization after SARS-Cov-2 infection generated Spike-specific classical memory B cells (MBCs) with low binding capacity to Spike protein and Spike-specific antibodies in a high percentage of CVID patients. The search for a strategy to elicit an adequate immune response post-vaccination in CVID patients is necessary. Since reinfection with SARS-CoV-2 has been documented, at present SARS-CoV-2 positive CVID patients might benefit from new preventing strategy based on administration of anti-SARS-CoV-2 monoclonal antibodies.

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“…However, many individuals severely affected by COVID-19 develop potent Tfh responses, implying that they also generate GC responses but still suffer from severe COVID-19 ( 259 ). Dysregulated T-cell responses likely play a role in this, but further investigations are required to explain the apparent heterogenous immunologic phenotype observed in severe COVID-19 ( 260 ).…”

Section: Adaptive Immune Response Against Sars-cov-2mentioning

confidence: 99%

Mechanistic Insights Into the Immune Pathophysiology of COVID-19; An In-Depth Review

Shafqat

Salameh

et al. 2022

Front. Immunol.

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Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), which causes coronavirus-19 (COVID-19), has caused significant morbidity and mortality globally. In addition to the respiratory manifestations seen in severe cases, multi-organ pathologies also occur, making management a much-debated issue. In addition, the emergence of new variants can potentially render vaccines with a relatively limited utility. Many investigators have attempted to elucidate the precise pathophysiological mechanisms causing COVID-19 respiratory and systemic disease. Spillover of lung-derived cytokines causing a cytokine storm is considered the cause of systemic disease. However, recent studies have provided contradictory evidence, whereby the extent of cytokine storm is insufficient to cause severe illness. These issues are highly relevant, as management approaches considering COVID-19 a classic form of acute respiratory distress syndrome with a cytokine storm could translate to unfounded clinical decisions, detrimental to patient trajectory. Additionally, the precise immune cell signatures that characterize disease of varying severity remain contentious. We provide an up-to-date review on the immune dysregulation caused by COVID-19 and highlight pertinent discussions in the scientific community. The response from the scientific community has been unprecedented regarding the development of highly effective vaccines and cutting-edge research on novel therapies. We hope that this review furthers the conversations held by scientists and informs the aims of future research projects, which will potentially further our understanding of COVID-19 and its immune pathogenesis.

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T cell immunity to SARS-CoV-2

Cited by 63 publications

References 125 publications

Limited induction of SARS-CoV-2–specific T cell responses in children with multisystem inflammatory syndrome compared with COVID-19

Limited induction of SARS-CoV-2–specific T cell responses in children with multisystem inflammatory syndrome compared with COVID-19

The Immune Response to SARS-CoV-2 Vaccination: Insights Learned From Adult Patients With Common Variable Immune Deficiency

Mechanistic Insights Into the Immune Pathophysiology of COVID-19; An In-Depth Review

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