Peripheral innate and adaptive immune cells during COVID-19: Functional neutrophils, pro-inflammatory monocytes, and half-dead lymphocytes.

BACKGROUND: A better understanding of innate and adaptive cells in COVID-19 is necessary for the development of effective treatment methods and vaccines. METHODS: We studied phenotypic features of innate and adaptive immune cells, oxidative burst, phagocytosis, and apoptosis. One hundred and three patients with COVID-19 were grouped according to their clinical features into the categories of mild (35%), moderate (40.8%), and severe (24.3%). RESULTS: Monocytes were CD16+ pro-inflammatory monocytes and tended to shed their HLA-DR, especially in severe cases (p < 0.01). Neutrophils were mature and functional, although a decline of their CD10 and CD16 was observed (p < 0.01). No defect was found in the reactive oxygen species production and their apoptosis. The percentage of natural killer cells was in the normal range, whereas the percentages of CD8+ NK and CD56+ T lymphocytes were found to be high (p < 0.01). Although the absolute numbers of all lymphocyte subsets were low and showed a tendency for a gradual decrease in accordance with the disease progression, the most decreased absolute number was that of B lymphocytes, followed by CD4+ T cells in the severe cases. The percentages of double-negative T cells; HLA-DR+ CD3+ and CD28- CD8+ subsets were found to be significantly increased. Importantly, we demonstrated the increased baseline activation of caspase-3 and increased lymphocyte apoptosis. CONCLUSION: We suggest that SARS-CoV-2 primarily affects the lymphocytes and not the innate cells. The increased baseline activation of Caspase-3 could make the COVID-19 lymphocytes more vulnerable to cell death. Therefore, this may interrupt the crosstalk between the adaptive and innate immune systems.

Pentraxin 3 and C-reactive protein as inflammatory markers after a kidney transplant.

OBJECTIVES: There are numerous changes in inflammatory status that occur after a kidney transplant. Pentraxin 3 is a marker of inflammation, but little information is available about pentraxin 3 levels after a kidney transplant. We evaluated the relation between pentraxin 3 and other inflammatory markers including high sensitivity C-reactive protein, interleukin 6, and tumor necrosis factor alpha in kidney transplant recipients. MATERIALS AND METHODS: Adult patients (40 patients; aged, 18-80 y; mean age, 38 ± 10 y) who had a kidney transplant from living-related donors were studied. Patients who had comorbidities associated with chronic inflammation were excluded. Blood samples were obtained before starting immunosuppressive treatment and 2 months after kidney transplant for measurement of pentraxin 3, high sensitivity C-reactive protein, interleukin 6, and tumor necrosis factor α levels. RESULTS: After transplant, mean levels of high sensitivity C-reactive protein and interleukin 6 decreased but levels of pentraxin 3 and tumor necrosis factor alpha did not change. There were significant correlations between interleukin 6 and high sensitivity C-reactive protein before transplant (r = 0.71; P ≤ .0001) and after transplant (r = 0.45; P ≤ .003). There was no correlation between tumor necrosis factor alpha and high sensitivity C-reactive protein before transplant, but there was a significant correlation between tumor necrosis factor alpha and high sensitivity C-reactive protein after transplant (r = 0.36; P ≤ .03). There was no correlation between interleukin 6 and pentraxin 3, tumor necrosis factor alpha and pentraxin 3, or high sensitivity C-reactive protein and pentraxin 3 before or after transplant. CONCLUSIONS: After a kidney transplant, pentraxin 3 may not be useful in determining inflammatory status, and high sensitivity C-reactive protein may be better than pentraxin 3 as a marker of inflammation.

A rare post-transplant malignancy, cerebellar hemangioblastoma: a case report.

INTRODUCTION: Post-transplant malignancies are among the most important complications in organ transplantation. Hemangioblastoma (HB) is especially prevalent in the cerebellum. CASE REPORT: A 20-year-old male who first started dialysis therapy, and then underwent kidney transplantation from a living-relative donor. Five years after transplantation, the patient suffered from vertigo and imbalance when walking. On cranial magnetic resonance imaging (MRI), a mass lesion in the right cerebellar hemisphere was observed, 3 x 3 x 3 cm in size, which was pushing against the fourth ventricle, and the right cerebellar peduncle. The patient had significant hydrocephaly. The mass lesion was removed by craniectomy. The pathological diagnosis was cerebellar hemangioblastoma. The symptoms and clinical findings improved. The patient was diagnosed with sporadic hemangioblastoma. Rapamycin therapy was started instead of cyclosporine, and the patient is being followed up without further problems. DISCUSSION: HB causes 2% of all intracranial tumors in the general population. It is generally sporadic in nature and approximately 20% can be associated with von Hippel-Lindau (VHL) syndrome. As in this case, MRI is preferred for the diagnosis. There was no pathology related to VHL disease in this patient's physical examination, family history, routine biochemical tests and abdominal MRI. The treatment is surgical excision of the tumor, as in this case. CONCLUSION: When cerebellar symptoms occur or a cerebellar mass lesion is detected in an organ recipient, HB should be considered in the differential diagnosis. The examination of patients with HB for a possible association with VHL disease is also required.