Background
Based on the fact that COVID-19 is still spreading despite vaccine worldwide administration, there is an imperative need to understand the underlying mechanisms of vaccine-induced inter-individual immune response variations.
Methods
We compared humoral and cellular immune responses in 127 individuals vaccinated with either BNT162b2, mRNA-1273 or ChAdOx1-nCoV-19 vaccine.
Results
We found that both mRNA vaccines induced faster and stronger humoral responses as assessed by high Spike- and RBD-specific antibody titers and neutralizing efficacy in comparison to ChAdOx1-nCoV-19 vaccine. At 7 months post vaccination, a decreasing trend in humoral responses was observed, irrespective of the vaccine administered. Correlation analysis between anti-S1 IgG and IFNγ production unveiled a heterogeneous immune profile among BNT162b2-vaccinated individuals. Specifically, vaccination in the high-responder group induced sizable populations of polyfunctional memory CD4+ TH1 cells, follicular helper T cells (TFH) and T cells with features of stemness along with high neutralizing antibody production that persisted up to 7 months.. In contrast, low responders were characterized by loss or significantly reduced antibody titers and memory T cells and a considerably lower capacity for IL-2 and IFNγ production.
Conclusions
We identified that long-term humoral responses correlate with the individual’s ability to produce antigen-specific persistent memory T cell populations.
Myasthenia gravis (MG) is an autoimmune disorder caused by autoantibodies targeting components of the postsynaptic membrane of the neuromuscular junction (NMJ), leading to neuromuscular transmission deficiency. In the vast majority of patients, these autoantibodies target the nicotinic acetylcholine receptor (nAChR), a heteropentameric ion channel anchored to the postsynaptic membrane of the NMJ. Autoantibodies in patients with MG may target all the subunits of the receptor at both their extracellular and intracellular regions. Here, we combine immunoadsorption with a cell-based assay to examine the specificity of the patients' autoantibodies against the extracellular part of the nAChR. Our results reveal that these autoantibodies can be divided into distinct groups, based on their target, with probably different impacts on disease severity. Although our findings are based on a small sample group of patients, they strongly support that additional analysis of the specificity of the autoantibodies of patients with MG could serve as a valuable tool for the clinicians' decision on the treatment strategy to be followed.
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