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1.
Front Immunol ; 13: 1030222, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-36389736

RESUMEN

The prognosis of human papillomavirus (HPV)-infected head and neck squamous cell carcinoma (HNSCC) is often better than that of HPV- cancer, which is possibly caused by the differences in their immune microenvironments. The contribution of macrophage, as a principal innate immune cell, to this phenomenon is still unclear. In this study, a single-cell atlas of 4,388 high-quality macrophages from 18 HPV- and 8 HPV+ HNSCC patients was constructed with single-cell RNA sequencing data. Eight macrophage subsets were identified from HNSCC, whereas their functional properties and developmental trajectory were delineated based on HPV status. Our results demonstrated that macrophages in HPV+ HNSCC exhibit stronger phagocytic ability, although the infiltration rate of macrophages decreased. From the results, a unique macrophage subset with TCR and CD3-specific signatures was identified from HPV-related HNSCC. These TCR+ macrophages potentially participate in the regulation of the TCR signaling pathway and phagocytosis. In conclusion, our results suggested that HPV could affect the infiltration rate, function, and differentiation of macrophages in HNSCC, whereas TCR+ macrophages play a critical role in the HNSCC microenvironment. These results provide new insights into the immune microenvironment of HNSCC and offer a valuable resource for the understanding of the immune landscape of HPV-related HNSCC, which will in turn help the development of immunotherapy strategies for the disease.


Asunto(s)
Carcinoma de Células Escamosas , Neoplasias de Cabeza y Cuello , Infecciones por Papillomavirus , Humanos , Carcinoma de Células Escamosas de Cabeza y Cuello , Neoplasias de Cabeza y Cuello/genética , Carcinoma de Células Escamosas/genética , Macrófagos , Análisis de Secuencia de ARN , Receptores de Antígenos de Linfocitos T/genética , Microambiente Tumoral
2.
Front Immunol ; 13: 880154, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-35898491

RESUMEN

Molecular assays on nasopharyngeal swabs act as a confirmatory test in coronavirus disease (COVID-19) diagnosis. However, the technical requirements of nasopharyngeal sampling and molecular assays limit the testing capabilities. Recent studies suggest the use of saliva for the COVID-19 diagnostic test. In this study, 44 patients diagnosed with COVID-19 in The Third People's Hospital of Shenzhen were enrolled. Saliva and serum specimens were obtained at different time points and the immunoglobulins against SARS-CoV-2 were measured. The results showed that saliva IgA presented a higher COI value than IgG and IgM. In matched saliva and serum samples, all saliva samples presented lower IgG levels than serum samples, and only one saliva sample presented a higher IgM level. The conversion rates of saliva IgA and the detection of viral nucleic acids were analyzed in the first and second weeks after hospitalization. The positive rates increased when combining saliva IgA and viral nucleic acid detection. In conclusion, our results provide evidence that saliva IgA could serve as a useful index for the early diagnosis of COVID-19.


Asunto(s)
COVID-19 , SARS-CoV-2 , Anticuerpos Antivirales , COVID-19/diagnóstico , Humanos , Inmunoglobulina A , Inmunoglobulina G , Inmunoglobulina M , Saliva
3.
Am J Cancer Res ; 11(9): 4380-4393, 2021.
Artículo en Inglés | MEDLINE | ID: mdl-34659893

RESUMEN

CSE1L is involved in the cancer progression of several types of cancer. Its expression status, potential oncogenic role and underlying mechanism in lung cancer, however, are unclear. Here, we investigated CSE1L expression in primary lung adenocarcinoma based on multiple datasets and then investigated its oncologic role in lung cancer. We also examined the potential molecular mechanisms of CSE1L in cancer progression. CSE1L levels were increased in cancer as compared to normal lung tissues. CSE1L expression was higher in poorly-differentiated late stage and lymph node positive metastatic tumors. Higher CSE1L level was correlated with worse patient outcome. Knockdown of CSE1L using siRNAs impaired cell proliferation, invasion, migration and induced cell apoptosis. Mechanistically, MET, STAT3 and PD-L1 proteins were decreased upon CSE1L silencing. These results suggest that CSE1L may affect tumor progression through MET/STAT3/PD-L1 signaling. CSE1L may have potential as a biomarker and therapeutic target for lung cancer.

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