Antiphospholipid syndrome (APS) is defined as an autoimmune and prothrombotic disorder in patients with the persistent presence of antiphospholipid antibodies (aPLs). In the classification criteria, aPL expresses lupus anticoagulant (LA) activity, which is detected by prolongation of coagulation assays. The LA detection algorithm is a sequential flow including screening tests, mixing tests, and confirmatory tests to differentiate between LA-positive and other anticoagulant abnormalities. Two types of assays are used, like dilute Russell’s viper venom time (dRVVT) and activated partial thromboplastin time (APTT) because no single test is sensitive to all LAs. The anticoagulant drugs prescribed for the prevention and treatment of thrombosis disorders can interfere with the assays, and it is important to know the effects of these drugs in the assays. Especially, new generation anticoagulant drugs, called direct oral anticoagulants (DOACs), affect the results. In this review, the following points are discussed: i) LA detection flow and data interpretation, ii) the principles of coagulation assays proposed and their characteristics, and iii) the effects of anticoagulant drugs in LA detection.

Vaccines are prophylactic medical products effectively used against infectious diseases. Although a high amount of vaccine studies are conducted at the preclinical stage, the number of approved vaccines is less than 10%. Development of vaccines from the research stage to the approval of administrative institutions takes about 5 years to 10 years conventionally. However, this period of time for vaccine development is not convenient during public health emergencies because an effective vaccine is required in a short time to restrict the speed of high mortality and morbidity. The pandemic of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), had its catastrophic effects worldwide quickly. Therefore, an atypical process was followed for the development of COVID-19 vaccines. Great effort was spent in terms of cooperation among the governmental institutions, academia, and medical companies as well as a high amount of budget was allocated to develop effective vaccines against COVID-19. As of March 2023, the numbers of COVID-19 vaccines in clinical and preclinical development were 183 and 199, respectively. An emergency use authorization (EUA) process was applied to accelerate the approval of the vaccines. Consequently, vaccinations could be started in less than a year, which decelerated the speed of the pandemic. Although EUA caused hesitancy among some people questioning the safety and efficacy of the vaccines, the vast majority of the population was vaccinated. Currently, more than 5.5 billion people (about 70% of the world population) have received 13.38 billion doses of 11 different COVID-19 vaccines, and 73% of the doses were Comirnaty manufactured by Pfizer/BioNTech.

Immunosenescence encompasses multiple age-related adaptations that result in increased susceptibility to infections, chronic inflammatory disorders, and higher mortality risk. Macrophages are key innate cells implicated in inflammatory responses and tissue homeostasis, functions progressively compromised by aging. This process coincides with declining mitochondrial physiology, whose integrity is required to sustain and orchestrate immune responses. Indeed, multiple insults observed in aged macrophages have been implied as drivers of mitochondrial dysfunction, but how this translates into impaired immune function remains sparsely explored. This review provides a perspective on recent studies elucidating the underlying mechanisms linking dysregulated mitochondria homeostasis to immune function in aged macrophages. Genomic stress alongside defective mitochondrial turnover accounted for the progressive accumulation of damaged mitochondria in aged macrophages, thus resulting in a higher susceptibility to excessive mitochondrial DNA (mtDNA) leakage and reactive oxygen species (ROS) production. Increased levels of these mitochondrial products following infection were demonstrated to contribute to exacerbated inflammatory responses mediated by overstimulation of NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome and cyclic GMP-ATP synthase (cGAS)-stimulator of interferon genes (STING) pathways. While these mechanisms are not fully elucidated, the present evidence provides a promising area to be explored and a renewed perspective of potential therapeutic targets for immunological dysfunction.

The etiology of recurrent spontaneous abortion (RSA) is extremely complex, as there are 40–50% of patients with unexplained miscarriages, known as unexplained RSA (URSA). URSA affects approximately 1–2% of females of childbearing age and has a massive impact on the physical and mental conditions of both patients and their families. The pathogenesis of the disease remains unclear, making its treatment complicated. In recent years, considerable progress has been made in the exploration of the URSA immune balance mechanism and it has been universally acknowledged that a balanced immune response (as abnormal immunity) may be the root cause of poor pregnancy outcomes. This review discussed and summarized the effects of immune cells and blocking antibodies (BAs) on URSA based on the current state of knowledge in this area. Additionally, molecular genetics also plays an essential role in the incidence rate of URSA since the role of genetic polymorphism in the pathogenesis of URSA has been thoroughly studied. Nonetheless, the outcomes of these studies are inconsistent, particularly across populations. This paper reviewed previous studies on URSA and maternal genetic polymorphism, focusing on and synthesizing the most important findings to date, and providing diagnostic recommendation for URSA patients with clinical symptoms.

Aim: The study aims to evaluate the incidence of recurrent thromboses in patients with primary antiphospholipid syndrome (PAPS) and its association with the presence of different antiphospholipid antibodies (aPLs) and known thrombogenic risk factors.

Methods: This retrospective study included 52 patients. The median age of the patients was 38.5 years [31.5; 43.5], and the duration of the disease was 9.0 years [3.1; 13.0]. aPLs, including IgG/IgM/IgA antibodies to cardiolipin (aCLs), IgG/IgM/IgA anti-beta2-glycoprotein I (anti-β₂-GPI), IgG anti-domain I-β₂-GPI (anti-β₂-GPIDI) antibodies, IgG/IgM antibodies to the phosphatidylserine/prothrombin complex (aPS/PT), and other thrombosis risk factors were included for analysis.

Results: Recurrent thrombosis was reported in 34 (65%) out of 52 patients and 18 (35%) did not have it. The main reason for the recurrence of thrombosis was the lack of anticoagulant therapy: in 18 (52.9%) out of 34 patients with recurrent thrombosis. Three patients were taking warfarin at the time of thrombosis recurrence, but target international normalized ratio (INR) levels were not achieved. Other patients with recurrent thrombosis were taking direct oral anticoagulants (DOACs). The risk of recurrent thrombotic events with positive IgG aCL was 10.33 ( P = 0.002) and 21 ( P = 0.007) times higher were examined in enzyme-linked immunoassay (ELISA) and chemiluminescent assay (CLA), respectively. The risk of thrombosis was 4.58 times higher in patients who were IgA aCL-positive ( P = 0.01). Compared with other antibodies, with positive IgG values of anti-β₂-GPI and IgG aPS/PT by ELISA, a lower probability of thrombosis recurrence was observed: 7.56 and 7.25, respectively. A high risk of recurrent thrombosis [odds ratio (OR) = 32.0] was observed in IgG anti-β₂-GPI (CLA). The combination of IgG aCL with IgG anti-β₂-GPI and with IgG anti-β₂-GPIDI is more informative with respect to the risks of thrombosis recurrence compared to double positivity for aCL with anti-β₂-GPI (OR = 20.71 vs. OR = 10.18). Triple positivity for IgG aCL with IgG anti-β₂-GPI and with IgG aPS/PT also shows better results compared to positivity for aCL with anti-β₂-GPI (OR = 6.06 vs. OR = 5.79). Among other risk factors, arterial hypertension (AH) and obesity were significant in relation to the recurrence of thrombosis. AH occurred in 22 (42%) of 52 patients with PAPS. AH was associated with recurrent thrombosis in PAPS patients: 18 (53%) out of 34 with recurrent thrombosis had AH versus 4 out of 18 without recurrent thrombosis ( P = 0.003).

Conclusions: Recurrent thrombosis in antiphospholipid syndrome (APS) is largely associated with IgG aCL, IgG anti-β₂-GPI, IgG anti-β₂-GPIDI, IgG aPS/PT, and IgA aCL positivity. AH was a significant risk factor for recurrent thrombosis.

One of the greatest challenges in the study of coronavirus disease 2019 (COVID-19) has been to establish the determining factors in the severity of the disease. Through extensive research efforts, a crucial factor responsible for disease control or exacerbation in COVID-19 has been identified-the regulation of the immune response. The abnormal release of interleukin-1 (IL-1), IL-6, and tumor necrosis factor-alpha (TNF-α) has been extensively studied in the context of the altered immune response observed in severe cases of COVID-19. However, recent attention has turned towards the excessive release of IL-17 and the increased presence of T helper 17 (Th17) cells, the main secretory cells of this cytokine. These factors have garnered interest due to their potential involvement in the cytokine storm observed in severe cases of COVID-19. In this review, it will be delved into the intricate mechanisms by which IL-6 contributes to the differentiation of Th17 cells, resulting in an increase in the population of Th17 cells. Moreover, it will be explored the proportional relationship between the increase of these lymphocytes and the release of IL-17 and other chemokines, which all together play a key role in promoting the chemotaxis and activation of neutrophils. Ultimately, this cascade of events culminates in the generation of tissue damage by neutrophils. Additionally, therapeutic options targeting these lymphocytes and cytokines are explored, providing insights into potential avenues for intervention.

Immunotherapeutic treatment of autoimmune diseases should aim to inactivate autoaggressive memory T-cells and restore immune tolerance. It is envisaged that three approaches could be used to achieve this goal: stimulation of anti-idiotypic immune responses by vaccination with pathogenic T-cells; administration of suboptimal doses of antibodies (Abs) against two or more surface T-cell markers to provide selective Ab-mediated destruction of activated pathogenic memory T-cells; and induction of oral immune tolerance. The proposal entails the use of T-cell vaccination (TCV) or Ab-based therapy as an initial approach to reduce autoantigenic T-cell sensitization. Subsequently, the implementation of oral immunotherapy (OIT) is recommended to reinstate a consistent immune tolerance.