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alphaB-crystallin is a novel biomarker expressed predominantly in triple negative breast tumors that identifies a subset of chemotherapy-resistant tumors, which may contribute to their poor prognosis.

Immunocompromised patients, including those with inborn errors of immunity (IEI), may be at increased risk for severe or prolonged infections with SARS-CoV-2 (Zhu et al. N Engl J Med. 382:727–33, 2020 ; Guan et al. 2020 ; Minotti et al. J Infect. 81:e61–6, 2020 ). While antibody and T cell responses to SARS-CoV-2 structural proteins are well described in healthy convalescent donors, adaptive humoral and cellular immunity has not yet been characterized in patients with antibody deficiency (Grifoni et al. Cell. 181:1489–1501 e1415, 2020 ; Burbelo et al. 2020 ; Long et al. Nat Med. 26:845–8, 2020 ; Braun et al. 2020 ). Herein, we describe the clinical course, antibody, and T cell responses to SARS-CoV-2 structural proteins in a cohort of adult and pediatric patients with antibody deficiencies ( n = 5) and controls (related and unrelated) infected with SARS-CoV-2. Five patients within the same family (3 with antibody deficiency, 2 immunocompetent controls) showed antibody responses to nucleocapsid and spike proteins, as well as SARS-CoV-2 specific T cell immunity at days 65–84 from onset of symptoms. No significant difference was identified between immunocompromised patients and controls. Two additional unrelated, adult patients with common variable immune deficiency were assessed. One did not show antibody response, but both demonstrated SARS-CoV-2-specific T cell immunity when evaluated 33 and 76 days, respectively, following SARS-CoV-2 diagnosis. This report is the first to show robust T cell activity and humoral immunity against SARS-CoV-2 structural proteins in some patients with antibody deficiency. Given the reliance on spike protein in most candidate vaccines (Folegatti et al. Lancet. 396:467–78, 2020 ; Jackson et al. N Engl J Med. 383:1920–31, 2020 ), the responses are encouraging. Additional studies will be needed to further define the timing of onset of immunity, longevity of the immune response, and variability of response in immunocompromised patients. Supplementary Information The online version contains supplementary material available at 10.1007/s10875-021-01046-y.

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Background Chronic rhinosinusitis (CRS) is a heterogeneous disease characterized by local inflammation of the upper airways and sinuses and is frequently divided into polypoid CRS (CRSwNP) and non-polypoid CRS (CRSsNP). However, the mechanism of inflammation in CRS has still not been fully elucidated. The aim of the study was to investigate the role of IL-32, a recently discovered proinflammatory cytokine, in CRS. Methods We collected nasal epithelial cells and nasal tissue from patients with CRS and control subjects. We assayed mRNA for IL-32 by real-time PCR and measured IL-32 protein by ELISA, western blot and immunohistochemistry. Results The expression of mRNA for IL-32 was elevated in epithelial cells from uncinate tissue from patients with CRSsNP compared to patients with CRSwNP (p<0.05), control subjects (p=0.06) or epithelial cells from nasal polyp tissue (p<0.05). Production of IL-32 was induced by IFN-γ, TNF and dsRNA in primary airway epithelial cells. In whole tissue extracts, the expression of IL-32 protein was significantly elevated in patients with CRSwNP compared to patients with CRSsNP and control subjects. Immunohistochemistry data showed that IL-32 was detected in mucosal epithelial cells and inflammatory cells in the lamina propria. Levels of IL-32 were correlated with levels of CD3 and macrophage mannose receptor in nasal polyp tissue. Immunofluorescence data showed IL-32 co-localization with CD3 positive T cells and CD68 positive macrophages in nasal polyps. Conclusion Overproduction of IL-32 may be involved in the pathogenesis of CRS, although the role of IL-32 in the inflammation in CRSsNP and CRSwNP may be different.