Fig 1: Both microglia and macrophages comprise the immune system in the cochlear sensory epithelium. (a) The Cd200-Cd200r1 system restricts microglial functions in the brain. Cd200 (green), the ligand of Cd200r1, was mainly expressed in HCs, but also weakly in SCs and GERCs. Cd200r1 (green) was expressed in SCs and GERCs. These findings indicate that Cd200-Cd200r1-specific intercellular signalling restricts SC/GERC functions to macrophages. During virus infection, Cd200r1 mRNA was significantly downregulated (Mock 9 h: n = 3, TMEV 9 h: n = 4, Mock 16 h: n = 4, TMEV 16 h: n = 3), despite little change in Cd200 expression (Mock 9 h: n = 3, TMEV 9 h: n = 4, Mock 16 h: n = 3, TMEV 16 h: n = 3) (*P < 0.05, **P < 0.01, t-test). These findings indicate that virus infection removes the Cd200-Cd200r1 restriction on SCs and GERCs, which induces their differentiation into macrophages. (b) In uninfected cochleae, Iba1-positive cells (green) were concentrically arranged beneath OPCs and DC1s, which might be cochlear resident microglia (arrowhead; outer PC: OPC, inner PC: IPC, DC1: first row of DCs, DC2: second row of DCs, DC3: third row of DCs). (c) Cochlear resident microglial cells were not observed in their original location during the virus infection. Scale bars, 20 µm. Error bars, standard errors.
Fig 2: The effect of MIA induced by LPS (a) and Poly I:C (b) treatment on the protein levels of CX3CL1, CX3CR1, CD200 and CD200R in the hippocampi (Hp) and the frontal cortices (Cx) of PND93 offspring. n = 6–8 in each group. The results are presented as the means ± SEMs. *p < 0.05 vs. appropriate control (kLPS or kPoly)
Fig 3: Immunohistofluorescent staining of CX3CL1-CX3CR1 (a, b) and CD200-CD200R (c, d) localization on neurons and microglial cells in the frontal cortex (Cx) of PND7 offspring after MIA induced by LPS treatment. Representative confocal images showing colocalization of CX3CL1/CD200 (red) immunoreactivity with MAP2 (green)-positive neurons and CX3CR1/CD200R (red) immunoreactivity with IBA1 (green)-positive microglial cells. n = 2 in each group. Magnification × 40 for all images. Scale bar (10 μm) is located in the bottom right corner of each image
Fig 4: The number of follicles at different stages, expression of CD200 and CD200R in EA-treated OHSS model. (A) The number of follicles at different stages in each group. (B) The ratio of corpora lutea/total follicles. (C) The protein expression of CD200 and CD200R in ovary of OHSS rats with or without EA treatment. (D) The CD200 levels in the serum of experimental groups were detected by ELISA. (E) The distribution of CD200 was detected by IHC, original magnification 40×, scale bar = 100 μm. Data were shown as means ± SD, *P < 0.5, **P < 0.01, ***P < 0.001 versus OHSS group.
Fig 5: The level of CD200 in follicular fluid and serum of patients who underwent IVF procedures. Correlations between CD200 concentration and the number of oocytes retrieved in FF (A) and serum (C) (n = 43). The levels of CD200 in follicular fluid (B) and serum (D) were compared between the groups with higher (≥18, n = 12), middle (6–17, n = 23), and lower (≤5, n = 8) oocytes retrieved. The correlations between CD200 concentration and the level of E2 and P were analyzed (E). ∗∗∗P < 0.001. Abbreviations: E2, estradiol; P, progesterone.
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