Background COVID-19 pneumonia may lead to pulmonary fibrosis in the long term. Chest CT is useful to evaluate changes in the lung parenchyma over time. Purpose To illustrate the temporal change of lung abnormalities on chest CT scans associated with COVID-19 pneumonia over 1 year. Materials and Methods In this prospective study, patients previously hospitalized due to COVID-19 pneumonia who visited the radiology department of a tertiary care center for imaging follow-up were consecutively enrolled between March 2020 and July 2021. Exclusion criteria were acute respiratory distress syndrome, requirement of intubation and/or mechanical ventilation, pulmonary embolism, and any interstitial lung disease. High-resolution volumetric noncontrast chest CT scans were acquired at 3, 6, and 12 months from the first diagnosis and were compared with baseline CT scans. The imaging features analyzed were ground-glass opacity (GGO), consolidation, pleuroparenchymal band, linear atelectasis, bronchiectasis and/or bronchiolectasis, reticulation, traction bronchiectasis and/or bronchiolectasis, and honeycombing. The prevalence distribution of lung abnormalities was recorded at all time points. Results Eighty-four participants (56 men; mean age, 61 years ± 11 [SD]) were studied. GGOs and consolidations represented the main baseline lung abnormalities, accounting for a median severity score of 9 (IQR, 7–12.7; maximum possible score, 20), which indicates moderate lung involvement. The baseline prevalence of GGOs decreased from 100% to 2% of participants at 1 year, and that of consolidations decreased from 71% to 0% at 6 months. Fibrotic-like abnormalities (pleuroparenchymal bands, linear atelectasis, bronchiectasis and/or bronchiolectasis) were detected at 3 months (50% of participants), 6 months (42% of participants), and 1 year (5% of participants). Among these, pleuroparenchymal bands were the most represented finding. Fibrotic changes (reticulation and traction bronchiectasis and/or bronchiolectasis) were detected at 3–6 months (2%) and remained stable at 1 year, with no evidence of honeycombing. At 1 year, lung abnormalities due to COVID-19 pneumonia were completely resolved in 78 of 84 (93%) participants. Conclusion Residual lung abnormalities in individuals hospitalized with moderate COVID-19 pneumonia were infrequent, with no evidence of fibrosis at 1-year chest CT. © RSNA, 2022

Coronavirus disease‐19 (COVID‐19) is a complex disorder caused by the pandemic diffusion of a novel coronavirus named SARS‐CoV‐2. Clinical manifestations vary from silent infection to severe pneumonia, disseminated thrombosis, multi‐organ failure, and death. COVID‐19 pathogenesis is still not fully elucidated, while increasing evidence suggests that disease phenotypes are strongly related to the virus‐induced immune system's dysregulation. Indeed, when the virus‐host cross talk is out of control, the occurrence of an aberrant systemic inflammatory reaction, named “cytokine storm,” leads to a detrimental impairment of the adaptive immune response. Dendritic cells (DCs) are the most potent antigen‐presenting cells able to support innate immune and promote adaptive responses. Besides, DCs play a key role in the anti‐viral defense. The aim of this review is to focus on DC involvement in SARS‐CoV‐2 infection to better understand pathogenesis and clinical behavior of COVID‐19 and explore potential implications for immune‐based therapy strategies.

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Idiopathic pulmonary fibrosis (IPF) is the most devastating progressive interstitial lung disease that remains refractory to treatment. Pathogenesis of IPF relies on the aberrant cross-talk between injured alveolar cells and myofibroblasts, which ultimately leads to an aberrant fibrous reaction. The contribution of the immune system to IPF remains not fully explored. Recent evidence suggests that both innate and adaptive immune responses may participate in the fibrotic process. Dendritic cells (DCs) are the most potent professional antigen-presenting cells that bridge innate and adaptive immunity. Also, they exert a crucial role in the immune surveillance of the lung, where they are strategically placed in the airway epithelium and interstitium. Immature DCs accumulate in the IPF lung close to areas of epithelial hyperplasia and fibrosis. Conversely, mature DCs are concentrated in well-organized lymphoid follicles along with T and B cells and bronchoalveolar lavage of IPF patients. We have recently shown that all sub-types of peripheral blood DCs (including conventional and plasmacytoid DCs) are severely depleted in therapy naïve IPF patients. Also, the low frequency of conventional CD1c+ DCs is predictive of a worse prognosis. The purpose of this mini-review is to focus on the main evidence on DC involvement in IPF pathogenesis. Unanswered questions and opportunities for future research ranging from a better understanding of their contribution to diagnosis and prognosis to personalized DC-based therapies will be explored.

Liquid biopsy, which allows the isolation of circulating cell-free (ccf) DNA from blood, is an emerging noninvasive tool widely used in oncology for diagnostic and prognosis purposes. Previous data have shown that serum cfDNA discriminates idiopathic pulmonary fibrosis (IPF) from other interstitial lung diseases. Our study aimed to measure plasma levels of ccfDNA in 59 consecutive therapy-naive and clinically stable IPF patients. The single nucleotide polymorphism (SNP) of the MUC5B gene promoter (rs35705950), associated with increased susceptibility of developing IPF, has been sought in plasma cfDNA and genomic DNA for comparison. Thirty-five age- and sex-matched healthy volunteers were recruited as the control group. Our results show that concentrations of small-size ccfDNA fragments were significantly higher in IPF patients than in controls and inversely correlated with lung function deterioration. Moreover, the median level of 104 ng/mL allowed discriminating patients with mild disease from those more advanced. The rs35705950 polymorphism was found in 11.8% of IPF patients and 8% of controls, with no differences. Complete concordance between ccfDNA and genomic DNA was detected in all control samples, while four out of seven IPF cases (57%) carrying the rs35705950 polymorphism were discordant from genomic DNA (7% of total IPF). Liquid biopsy is a suitable tool with optimistic expectations of application in the field of IPF. In analogy with cancer biology, finding some discrepancies between ccfDNA and genomic DNA in IPF patients suggests that the former may convey specific genetic information present in the primary site of the disease.