Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 4 de 4
Filter
1.
Ann Allergy Asthma Immunol ; 130(6): 743-751.e3, 2023 06.
Article in English | MEDLINE | ID: covidwho-2278785

ABSTRACT

BACKGROUND: Clinical trials of the mRNA coronavirus disease 2019 (COVID-19) vaccines excluded individuals with primary antibody deficiencies. OBJECTIVE: To evaluate whether antibody and T-cell responses to mRNA COVID-19 vaccination in patients with common variable immunodeficiency (CVID) and specific antibody deficiency (SAD) were comparable to those in healthy controls. METHODS: We measured antibody responses against the spike glycoprotein and the receptor-binding domain (RBD) in addition to severe acute respiratory syndrome coronavirus 2 specific T-cell responses using peripheral blood mononuclear cells 2 to 8 weeks after the subjects completed the primary 2-dose vaccine series. RESULTS: The study comprised 12 patients with CVID, 7 patients with SAD, and 10 controls. Individuals with CVID had lower immunoglobulin (Ig) G and Ig A levels against spike glycoprotein than did both individuals with SAD (P = .27 and P = .01, respectively) and controls (P = .01 and P = .004, respectively). The CVID group developed lower IgG titers against the RBD epitope than did the control group (P = .01). Participants with CVID had lower neutralizing titers than did the control group (P = .002). All participants with SAD developed neutralizing titers. All 3 groups (SAD, CVID, and control) developed antigen-specific CD4+ and CD8+ T-cell responses after vaccination. CONCLUSION: Our results suggest that patients with CVID may have impaired antibody responses to COVID-19 vaccination but intact T-cell responses, whereas patients with SAD would be expected to have both intact antibody and T-cell responses to vaccination.


Subject(s)
COVID-19 , Common Variable Immunodeficiency , Primary Immunodeficiency Diseases , Humans , COVID-19/prevention & control , COVID-19 Vaccines , Leukocytes, Mononuclear , Vaccination , Immunoglobulin G , Glycoproteins
2.
Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology ; 2023.
Article in English | EuropePMC | ID: covidwho-2235007

ABSTRACT

Background Clinical trials of the mRNA COVID-19 vaccines excluded individuals with primary antibody deficiencies. Objective The aim of this study was to evaluate whether antibody and T-cell responses to mRNA COVID-19 vaccination in patients with Common Variable Immunodeficiency (CVID) and Specific Antibody Deficiency (SAD) were comparable to healthy controls. Methods We measured antibody responses against the S protein and the receptor binding domain (RBD) as well as SARS-CoV2 specific T-cell responses using peripheral blood mononuclear cells (PBMCs) 2-8 weeks after subjects completed the primary 2-dose vaccine series. Results 12 patients with CVID, 7 patients with SAD, and 10 controls were included in the study. Individuals with CVID had lower IgG and IgA levels against S protein compared to both individuals with SAD (p= 0.27 and p=0.01, respectively) and as well as to controls (p=0.012 and p=0.004, respectively). The CVID group developed lower IgG titers against the RBD epitope compared to the control group (p=0.014). CVID participants had lower neutralizing titers compared to the control group (p=0.002). All SAD participants developed neutralizing titers. All three of our groups (SAD, CVID, and control) developed antigen-specific CD4+ and CD8+ T-cell responses after vaccination. Conclusion Our results suggest that patients with CVID may have impaired antibody responses to COVID-19 vaccination but intact T-cell responses, while patients with SAD would be expected to have both intact antibody and T-cell responses to vaccination.

3.
Front Immunol ; 13: 819574, 2022.
Article in English | MEDLINE | ID: covidwho-2121729

ABSTRACT

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 is a complex disease which immune response can be more or less potent. In severe cases, patients might experience a cytokine storm that compromises their vital functions and impedes clearance of the infection. Gamma delta (γδ) T lymphocytes have a critical role initiating innate immunity and shaping adaptive immune responses, and they are recognized for their contribution to tumor surveillance, fighting infectious diseases, and autoimmunity. γδ T cells exist as both circulating T lymphocytes and as resident cells in different mucosal tissues, including the lungs and their critical role in other respiratory viral infections has been demonstrated. In the context of SARS-CoV-2 infection, γδ T cell responses are understudied. This review summarizes the findings on the antiviral role of γδ T cells in COVID-19, providing insight into how they may contribute to the control of infection in the mild/moderate clinical outcome.


Subject(s)
COVID-19 , Immunity, Innate , T-Lymphocyte Subsets , Antiviral Agents , COVID-19/immunology , Cytokines , Humans , Receptors, Antigen, T-Cell, gamma-delta , SARS-CoV-2 , T-Lymphocyte Subsets/immunology
4.
Int J Mol Sci ; 23(4)2022 Feb 19.
Article in English | MEDLINE | ID: covidwho-1715402

ABSTRACT

Platelets, which are small anuclear cell fragments, play important roles in thrombosis and hemostasis, but also actively release factors that can both suppress and induce viral infections. Platelet-released factors include sCD40L, microvesicles (MVs), and alpha granules that have the capacity to exert either pro-inflammatory or anti-inflammatory effects depending on the virus. These factors are prime targets for use in extracellular vesicle (EV)-based therapy due to their ability to reduce viral infections and exert anti-inflammatory effects. While there are some studies regarding platelet microvesicle-based (PMV-based) therapy, there is still much to learn about PMVs before such therapy can be used. This review provides the background necessary to understand the roles of platelet-released factors, how these factors might be useful in PMV-based therapy, and a critical discussion of current knowledge of platelets and their role in viral diseases.


Subject(s)
Blood Coagulation Factors/metabolism , Blood Platelets/metabolism , Extracellular Vesicles/metabolism , Virus Diseases/metabolism , Animals , Cell-Derived Microparticles/metabolism , Humans , Platelet Activation/physiology
SELECTION OF CITATIONS
SEARCH DETAIL