Granulomatous orchitis: A case report of misdiagnosis and review of the literature.

Granulomatous orchitis is a relatively rare clinical testicular lesion. The imaging manifestations and clinical symptoms are similar to those of testicular tumors. In order to improve the understanding of this disease, this article reports the ultrasonographic manifestations of a case of granulomatous orchitis and reviews the relevant literature with.

Foxp3-mediated blockage of ryanodine receptor 2 underlies contact-based suppression by regulatory T cells.

The suppression mechanism of Tregs remains an intensely investigated topic. As our focus has shifted toward a model centered on indirect inhibition of DCs, a universally applicable effector mechanism controlled by the transcription factor forkhead box P3 (Foxp3) expression has not been found. Here, we report that Foxp3 blocked the transcription of ER Ca2+-release channel ryanodine receptor 2 (RyR2). Reduced RyR2 shut down basal Ca2+ oscillation in Tregs, which reduced m-calpain activities that are needed for T cells to disengage from DCs, suggesting a persistent blockage of DC antigen presentation. RyR2 deficiency rendered the CD4+ T cell pool immune suppressive and caused it to behave in the same manner as Foxp3+ Tregs in viral infection, asthma, hypersensitivity, colitis, and tumor development. In the absence of Foxp3, Ryr2-deficient CD4+ T cells rescued the systemic autoimmunity associated with scurfy mice. Therefore, Foxp3-mediated Ca2+ signaling inhibition may be a central effector mechanism of Treg immune suppression.

Circular RNA SMEK1 promotes neuropathic pain in rats through targeting microRNA-216a-5p to mediate Thioredoxin Interacting Protein (TXNIP) expression.

Neuropathic pain (NP) is a disease induced by damage to the nervous system. A large number of studies have manifested that circular RNAs (circRNAs) are key in the development of neurological diseases. However, the role of circRNA in NP remains ambiguous. In this study, the biological function and molecular mechanism of circSMEK1 were investigated in NP. NP rat and cell models were established by chronic contractile injury (CCI) surgery and lipopolysaccharide (LPS) treatment, separately. The results exposed that circSMEK1 and TXNIP were up-regulated in NP, while miR-216a-5p was down-regulated. The claw retraction threshold and claw retraction latency in rats were elevated and reduced separately via knockdown circSMEK1 and miR-216a-5p. Meanwhile, knockout circSMEK1 or elevated miR-216a-5p declined inflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß and IL6 in spinal cord, and the activation of microglia, but promoted the polarization of microglia into anti-inflammatory type, while up-regulation of circSMEK1 or knockdown of miR-216a-5p was opposite. Mechanism studies demonstrated that circSMEK1 mediated TXNIP expression through competitive adsorption of miR-216a-5p. Functional rescue experiments manifested that the suppressive effect of circSMEK1 knockdown on NP was reversed by declined miR-216a-5p simultaneously. In conclusion, the results of this study affirmed that circSMEK1 facilitates NP inflammation and microglia M1 polarization by modulating miR-216a-5p/TXNIP axis, providing a new molecular target for the future treatment of NP.