Clinical Immunology Communications最新文献

Despite the great impact of severe acute respiratory syndrome caused by coronavirus 2 (SARS-CoV-2), we still lack techniques that allow us to anticipate the natural history of the disease in order to avoid or shorten the clinical period of the disease. The values of nine cytokines were measured in COVID-19+ patients admitted to the Hospital Universitario Reina Sofía (HURS) using flow cytometry. The cytokines measured are IL-1ß, IL-6, MCP-1, IP-10, IL-10, IL-8, IL-12, IFN-γ and TNF-α. Given the absence of previous studies on cytokine values in healthy patients using the flow cytometry technique, and the low availability of resources in the first waves of COVID-19, a control group was lacking, all resources were employed for monitoring sick patients. However, this study has revealed a greater increase in two specific cytokines, which are also found to be higher than the rest in healthy patients: MCP-1 and IP-10, which are mainly responsible for cytokine storm and post-disease thrombosis.

Host-defense peptides (HDPs) such as human beta-defensin-2 (hBD-2) and cathelicidin (LL37) are essential components of innate immune response against tuberculosis (TB) infection, which could also be assessed for diagnostic potential in spectrum of TB infection. We assessed mRNA and circulating levels of HDPs in pulmonary TB (PTB) patients and their household contacts (HHCs). hBD-2 and LL37 were found to be significantly higher in both PTB and HHCs suggestive of bacterial exposure which was further corroborated by higher levels of HDPs in mantoux positive HHCs (latent TB). Higher levels of HDPs in HHCs may suggest protective host response against infection as indicated by inverse relation of LL37 with disease severity in PTB. Both peptides demonstrated high levels of sensitivity and specificity, although hBD-2 proved to be a better HDP for distinguishing LTBI from active TB at a cutoff of 3904 pg/ml. However, follow-up studies are required to validate these findings.

In the aging population, the longitudinal decrease in the secretion of steroidal and polypeptides growth hormones is directly associated with accumulation of senescent cells in tissues and organs. The cellular hypo-replicative senescence state is caused by metabolic stress and persistent DNA damage, which lead to the activation of the p16^INK4a cell-cycle inhibitor, retinoblastoma and p53 pathways. Aging increases the susceptibility to physical frailty, sarcopenia, diabetes, atherosclerosis, infectious disease and cancer in the older adults. As a consequence of immunosenescence and reduced immunoreactivity of the innate and adaptive systems, seniors have a weak response to vaccination. The high doses of vaccines have been recommended to boost growth and activation of memory T and B cells in non-responsive older individuals, but it is not sufficient for long-term protection. The treatment with recombinant human growth hormone has been shown to regenerate thymus and increase the repertoire of naive T cells CD4+ and CD8+ T cell and B cell subsets in people with age-related diseases, chronic viral infection and immunodeficiencies. This review presents an update on senescence biology and their clinical immunological manifestations in the elderly. We describe possible immune mechanisms by which personalized recombinant growth hormone therapy could act to prolong the effectiveness of the vaccines recommended to older adults.

We analyzed immune response to SARS-CoV-2 vaccination by measuring specific IgG titers and T-cell reactivity to different SARS-CoV-2 peptides in multiple sclerosis patients taking different disease-modifying treatments. Of the 88 patients included, 72 developed any kind of immune response after vaccination. Although DMTs such as fingolimod and anti-CD20+ treatments prevented patients from developing a robust humoral response to the vaccine, most of them were still able to develop a cellular response, which could be crucial for long-term immunity. It is probably advisable that all MS patients take additional/booster doses to increase their humoral and/or cellular immune response to SARS-CoV-2.

The pandemic caused by the SARS-CoV-2 coronavirus has been especially detrimental to patients with end-stage renal disease. History with other vaccines suggests that patients with renal disease may not respond adequately to the SARS-CoV-2 vaccine. The aim of this study is to evaluate the immunity to SARS-CoV-2 mRNA vaccines in renal patients. Post SARS-CoV-2 vaccination first, and after the booster dose, antibodies and cellular immunity were studied in patients on hemodialysis (N = 20), peritoneal dialysis (N = 10) and renal transplantation (N = 10). After the two doses of vaccine, there was an effective immunity in dialysis patients, with 100% seroconversion and 87% detection of cellular immunity (85% in hemodialysis and 90% in peritoneal dialysis). In contrast, in renal transplant recipients there was only 50% seroconversion and cellular immunity was detected in 30% of patients. After the booster dose, all dialysis patients achieved a cellular and antibody immunity, whereas in transplant patients, despite improvement, 20% did not produce antibodies and in 37.5% cellular immunity could not be detected. The mRNA vaccine plus booster performs excellently in dialysis patients, whereas in kidney transplant recipients, despite the booster, complete immunization is not achieved.

Passive immunization with mAbs has been employed in COVID-19. We performed a systematic review of the literature assessing the endogenous humoral immune response against SARS-CoV-2 in patients treated with mAbs. Administration of mAbs in seronegative patients led to a reduction in both antibody titres and neutralizing activity against the virus.

The decline in vaccine efficacy and the risk of reinfection by SARS-CoV-2 make new studies important to better characterize the immune response against the virus and its components. Here, we investigated the pattern of activation of T-cells and the expression of inflammatory factors by PBMCs obtained from naïve and previously infected subjects following COVID-19 vaccination, after PBMCs stimulation with S1, RBD, and N-RBD SARS-CoV-2 proteins. PBMCs showed low levels of ACE2 and TMPRSS2 transcripts, which were not modulated by the exposure of these cells to SARS-CoV-2 proteins. Compared to S1 and RBD, N-RBD stimulation showed a greater ability to stimulate T-cell reactivity, according to CD25 and CD69 markers. Interestingly, T-cell reactivity was more pronounced in vaccinated subjects with prior SARS-CoV-2 infection than in vaccinated donors who never had been diagnosed with COVID-19. Finally, N-RBD stimulation promoted greater expression of IL-6 and IFN-γ in PBMCs, which reinforces the greater immunogenic potential of this protein in the vaccinated subjects. These data suggest that PBMCs from previously infected and vaccinated subjects are more reactive than those derived from just vaccinated donors. Moreover, the N-RBD together viral proteins showed a greater stimulatory capacity than S1 and RBD viral proteins.

Introduction: The AbC-19™ lateral flow immunoassay (LFIA) performance was evaluated on plasma samples from a SARS-CoV-2 vaccination cohort, WHO international standards for anti-SARS-CoV-2 IgG (human), individuals ≥2 weeks from infection of RT-PCR confirmed SARS-CoV-2 genetic variants, as well as microorganism serology.

Methods: Pre-vaccination to three weeks post-booster samples were collected from a cohort of 111 patients (including clinically extremely vulnerable patients) from Northern Ireland. All patients received Oxford-AstraZeneca COVID-19 vaccination for the first and second dose, and Pfizer-BioNTech for the third (first booster). WHO international standards, 15 samples from 2 variants of concern (Delta and Omicron) and cross-reactivity with plasma samples from other microorganism infections were also assessed on AbC-19™.

Results: All 80 (100%) participants sampled post-booster had high positive IgG responses, compared to 38/95 (40%) participants at 6 months post-first vaccination. WHO standard results correlated with information from corresponding biological data sheets, and antibodies to all genetic variants were detected by LFIA. No cross-reactivity was found with exception of one (of five) Dengue virus samples.

Conclusion: These findings suggest BNT162b2 booster vaccination enhanced humoral immunity to SARS-CoV-2 from pre-booster levels, and that this antibody response was detectable by the LFIA. In combination with cross-reactivity, standards and genetic variant results would suggest LFIA may be a cost-effective measure to assess SARS-CoV-2 antibody status.

The 2019 Coronavirus disease (COVID-19) vaccine is a major weapon in the fight against the severe acute respiratory syndrome brought about by coronavirus 2 (SARS-CoV-2). The vaccine significantly reduces the risk and severity of infection by SARS-CoV-2. Patients with systemic lupus erythematosus (SLE) need protection from vaccine-preventable diseases including COVID-19. SLE patients have higher rates of severe infections due to immunosuppressive therapies and multiple immunologic defects – both of which are capable of blunting the immune responses after vaccination. In the management of COVID-19, recommendations have been developed to guide adjustments and/or continuation of immunosuppressive therapies for an effective immune response following vaccination with mRNA-based or viral vector-delivered vaccines. Monoclonal antibodies have also become available since December 2021. Here we present three cases of SLE patients who contracted COVID-19 after vaccination. One was managed in ambulatory settings and two required inpatient hospital admission.