Most of the mammalian follicles undergo a degenerative process called “follicle atresia”. Apoptosis of granulosa cells is the main characteristic of follicle atresia. Follicle stimulating hormone (FSH) and the transforming growth factor β (TGF-β) superfamily have important regulatory functions in this process. FSH activates protein kinase A and cooperating with insulin receptor substrates, it promotes the PI3K/Akt pathway which weakens apoptosis. Both Smad or non-Smad signaling of the transforming growth factor β superfamily seem to be related to follicle atresia, and the effect of several important family members on follicle atresia is concluded in this article. FSH and TGF-β are likely to mutually influence each other and what we have already known about the possible underlying molecular mechanism is also discussed below.
T follicular helper (Tfh) cells and T follicular regulatory (Tfr) cells are identified as the new subset of immune cells. This study aims to investigate the role of circulating Tfh cells (cTfh) and Tfr (cTfr) cells in the pathogenesis of non-small cell lung cancer (NSCLC). A total of 27 NSCLC patients and 19 age and sex-matched healthy controls were enrolled. The percentage of cTfh and cTfr was detected by flow cytometric analysis. Compared to healthy controls, a significantly higher percentage of both cTfh and cTfr cells were observed in NSCLC patients (for cTfh, 18.88% ± 16.84% versus 5.98% ± 3.70%, P < 0.01; for cTfr, 2.67% ± 2.20% versus 1.14% ± 0.76%, P < 0.01). Furthermore, there was a positive correlation between cTfh/cTfr ratio and age in NSCLC patients (P < 0.05). When taking age 60 as a cut-off, the percentage of both cTfh cells and cTfr cells were higher in older patients than younger patients. Moreover, our data showed there was lower percentage of cTfh cells in NSCLC patients with early stage disease (I and II) (12.10% ± 12.22%) than that in advanced stage disease (III and IV) (30.41% ± 17.87%) (P < 0.01). However, no significant relationship was observed between cTfr cells and clinical stage in NSCLC patients. A higher percentage of cTfh cells was observed in patients with squamous cell carcinoma compared with adenocarcinoma (31.70% ± 20.73% versus. 13.48% ± 11.78%, P < 0.05). Taken together, there was significantly higher percentage of cTfh and cTfr cells in NSCLC patients. cTfh and cTfr cells might play an important role in the pathogenesis of NSCLC patients.
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