Image_1_Increased histone H3 acetylation inhibit the inflammatory response and activate the serum immunity of Pearl oyster Pinctada fucata martensii.tif

To produce cultured pearls, a mantle graft with a nucleus is transplanted into a host pearl oyster, this process is called “transplantation”. The immune response of pearl oyster after transplantation is a major factor that leads to nucleus rejection and death. Butyrate is a histone deacetylase (HDAC) inhibitor which can inhibit the deacetylation process of histones and effectively reduce the inflammatory response. To clarify the function of histone acetylation in immune response after transplantation, butyrate (10 mmol/L) was used for the treatment of pearl oysters before transplantation. Results showed that the proportion of histone H3 acetylation of the hemocytes was significantly increased after butyrate treatment before transplantation (BH group) compared with the control group at 6–24 h. Transcriptome analysis showed that butyrate treatment activated the “lysosome”, inhibited cell migration and cell proliferation at 6 and 12 h, respectively, and activated the intracellular immune recognition response of pearl oyster at 24 h after transplantation. The apoptosis detection revealed no significant difference in the proportion of apoptotic cells between the control and BH group. Moreover, butyrate treatment increased the activity of some immune-related enzymes in the serum of pearl oyster after transplantation.</p

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Additional file 3: Figure S3. Multi-alignment of alpha nAChR genes from H. sapiens

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Additional file 2: Figure S2. Multi-alignment of Cys-loop of nAChR genes from C. gigas and H. sapiens

MOESM1 of Massive expansion and diversity of nicotinic acetylcholine receptors in lophotrochozoans

Additional file 1: Figure S1. Extron-intron structure of nAChR genes from H. sapiens

Image_2_Increased histone H3 acetylation inhibit the inflammatory response and activate the serum immunity of Pearl oyster Pinctada fucata martensii.tif

To produce cultured pearls, a mantle graft with a nucleus is transplanted into a host pearl oyster, this process is called “transplantation”. The immune response of pearl oyster after transplantation is a major factor that leads to nucleus rejection and death. Butyrate is a histone deacetylase (HDAC) inhibitor which can inhibit the deacetylation process of histones and effectively reduce the inflammatory response. To clarify the function of histone acetylation in immune response after transplantation, butyrate (10 mmol/L) was used for the treatment of pearl oysters before transplantation. Results showed that the proportion of histone H3 acetylation of the hemocytes was significantly increased after butyrate treatment before transplantation (BH group) compared with the control group at 6–24 h. Transcriptome analysis showed that butyrate treatment activated the “lysosome”, inhibited cell migration and cell proliferation at 6 and 12 h, respectively, and activated the intracellular immune recognition response of pearl oyster at 24 h after transplantation. The apoptosis detection revealed no significant difference in the proportion of apoptotic cells between the control and BH group. Moreover, butyrate treatment increased the activity of some immune-related enzymes in the serum of pearl oyster after transplantation.</p

DataSheet1_Immune Classification and Immune Landscape Analysis of Triple-Negative Breast Cancer.ZIP

Background: To classify triple-negative breast cancer (TNBC) immunotyping using the public database, analyze the differences between subtypes in terms of clinical characteristics and explore the role and clinical significance of immune subtypes in TNBC immunotherapy.Methods: We downloaded TNBC data from the cBioPortal and GEO databases. The immune genes were grouped to obtain immune gene modules and annotate their biological functions. Log-rank tests and Cox regression were used to evaluate the prognosis of immune subtypes (IS). Drug sensitivity analysis was also performed for the differences among immune subtypes in immunotherapy and chemotherapy. In addition, dimension reduction analysis based on graph learning was utilized to reveal the internal structure of the immune system and visualize the distribution of patients.Results: Significant differences in prognosis were observed between subtypes (IS1, IS2, and IS3), with the best in IS3 and the worst in IS1. The sensitivity of IS3 to immunotherapy and chemotherapy was better than the other two subtypes. In addition, Immune landscape analysis found the intra-class heterogeneity of immune subtypes and further classified IS3 subtypes (IS3A and IS3B). Immune-related genes were divided into seven functional modules (The turquoise module has the worst prognosis). Five hub genes (RASSF5, CD8A, ICOS, IRF8, and CD247) were screened out as the final characteristic genes related to poor prognosis by low expression.Conclusions: The immune subtypes of TNBC were significantly different in prognosis, gene mutation, immune infiltration, drug sensitivity, and heterogeneity. We validated the independent role of immune subtypes in tumor progression and immunotherapy for TNBC. This study provides a new perspective for personalized immunotherapy and the prognosis evaluation of TNBC patients in the future.</p

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Additional file 7: Table S1. Expression of nAChR genes (RPKM > 1) in different organs and at different development stages in C. gigas and P. f. martensii

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Additional file 5: Figure S5. Expression of six nAChR genes in gills of C. gigas under different environmental conditions (data from Zhang et al. 2012). a Seven days at 5–25 °C or 12 h at 30 and 35 °C; b Seven days under different salinities; and c Air exposure for different durations

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Additional file 4: Figure S4. Sequence diversity at and around ACh binding sites in 33 nAChR genes of C. gigas with the sites conserved. Sequences marked by the red underline is the Cys-loop. Amino acids in green boxes are ACh binding sites. Hsa, H. sapiens; Tma, Torpedo marmorata. Genes in purple are nAChRs with completely conserved principal binding sites

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Additional file 6: Figure S6. Expression of nAChR genes in gills of C. gigas in response to infection by pathogens. Left, expression of 3 nAChRs at different times after Vibrio (V. anguillarum, V. tubiashii, V. aestuarianus, V. alginolyticus) challenge (data from Zhang et al. 2015); Right, expression of 3 nAChRs at different times after Ostreid herpesvirus 1-μVar challenge (data from He et al. 2015). Y-axes is expression relative to Time 0