SUMMARYActivated dendritic cells are critically important in the priming of T-cell responses. In this report we show that the infection of a conditionally immortalized dendritic cell line (tsDC) with Mycobacterium tuberculosis resulted in the up-regulation of B7-1 and B7-2 co-stimulatory molecules and the induction of several in¯ammatory cytokines, including tumour necrosis factor-a and interleukin-6, -1b and -12. In addition, we show that these activated dendritic cells were capable of eliciting antigen-speci®c T-cell responses and potent anti-mycobacterial protective immunity in a murine model of experimental tuberculosis infection.

In the past 20 years, the platelet concentrates have evolved from first-generation products, i.e., platelet-rich plasma (PRP) and plasma rich in growth factors to the second-generation products such as leukocyte-platelet-rich fibrin (L-PRF) and advanced platelet-rich fibrin (A-PRF). These autologous products with a higher leukocyte inclusion and flexible fibrin mesh act as a scaffold to increase cellular migration in the angiogenic, osteogenic, and antimicrobial potential of these biomaterials in tissue regeneration. In the second-generation platelet concentrates, the protocols are easier, cheaper, and faster with an entire physiological fibrin matrix, resulting in a tridimensional mesh, not as rigid as one of the first generations. This allows the slow release of molecules over a longer period of time and triggers the healing and regenerative process at the site of injury. The potential of A-PRF to mimic the physiology and immunology of wound healing is also due to the high concentration of growth factors released as follows: vascular endothelial growth factor, platelet-derived growth factor, transforming growth factor-β, and anti-inflammatory cytokines that stimulate tissue cicatrization, vessels formation, and bone cell proliferation and differentiation. Furthermore, the number of neutrophils and monocytes/macrophages is higher releasing important chemotactic molecules such as chemokine ligand-5 and eotaxin. Thus, L-PRF and A-PRF have been used, especially in implantology, periodontology, and maxillofacial surgery. Future clinical applications include tissue regeneration/grafts, ulcers/skin necrosis in the diabetic patient and others, plastic surgery, and even musculoskeletal lesions.

Cardiovascular diseases (CVDs) are responsible for a high mortality rate worldwide. One of the most common causes of CVDs is vascular inflammation associated to atherosclerosis. Inflammatory biomarkers are used to assist the detection of CVDs and monitor their evaluation, prognosis and therapy implementation. C-reactive protein (CRP) is an acute phase protein produced after stimulation by pro-inflammatory cytokines. CRP is a biomarker of the inflammatory reaction and an important mediator of atherosclerosis. Given it actively contributes to the development of the atherosclerotic plaque, instability and subsequent clot formation it is also considered a CVD risk factor. Since 2010, the plasma concentration of hsCRP (high sensitivity CRP) has been used as a biomarker for disease prognosis in patients with intermediate risk for CVDs. It could be useful to establish a high concentration limit of hsCRP that can be used by clinicians for diagnosis of acute myocardial infarction, cardio embolic or ischemic stroke, and hypertrophic cardiomyopathy. The end cost/effectiveness of hsCRP screening is still an area of controversy but it is a priority to make the medical community aware of the positive relation between high hsCRP and CVDs to improve median survival and life quality of the patients.

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The purpose of this work was to analyse published data on rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and multiple sclerosis (MS) and SARS-CoV-2 infection: susceptibility, post-infection autoimmune disease (AD) exacerbation, immunosuppressive therapies and long COVID. Supported by PICO strategy, two independent reviewers conducted the research in the PubMed/Medline database from January 2020 to June 2022 and included 16 articles on RA, 25 on MS and 12 on SLE. The quality assessment of the studies was performed using criteria from the National Institute of Health. Patients with RA or SLE had increased susceptibility to contracting SARS-CoV-2. It was higher in RA and increased with the patients’ comorbidities. For MS, susceptibility to SARS-CoV-2 was similar to the general population. Post-infection AD exacerbation occurred in AR, SLE and MS with an increased number of hospitalisations and deaths. Regarding therapies, in RA the use of glucocorticoids (GC) was associated with a worsening of the infection. A more severe clinical picture was associated with anti-CD20 in SLE and with anti-CD20 and methylprednisolone in MS. Considering long COVID, RA and SLE patients had a higher risk of complications opposite to MS patients. There was a higher susceptibility to SARS-CoV-2 infection in rheumatological diseases AR and SLE, exacerbated by age and comorbidities. For RA and MS, GC aggravated the infection and for SLE and MS anti-CD20 antibodies use. In all AD there was exacerbation and worsening of the clinical picture translated in long COVID, the latter with MS exception.