http://localhost:8080/xmlui/handle/123456789/9071 2026-04-08T23:14:10Z http://localhost:8080/xmlui/handle/123456789/9220 Title: Inhibition of NK cell cytotoxicity by tubular epithelial cell expression of Clr-b and Clr-f Authors: Fuhrmann, Benjamin; Jiang, Jifu; Mcleod, Patrick Abstract: NK cells participate in ischemia reperfusion injury (IRI) and transplant rejection. Endogenous regulatory systems may exist to attenuate NK cell activation and cytotoxicity in IRI associated with kidney transplantation. A greater understanding of NK regulation will provide insights in transplant outcomes and could direct new therapeutic strategies. Kidney tubular epithelial cells (TECs) may negatively regulate NK cell activation by their surface expression of a complex family of C-type lectin-related proteins (Clrs). We have found that Clr-b and Clr-f were expressed by TECs. Clr-b was upregulated by inflammatory cytokines TNFα and IFNγ in vitro. Silencing of both Clr-b and Clr-f expression using siRNA resulted in increased NK cell killing of TECs compared to silencing of either Clr-b or Clr-f alone (p < 0.01) and when compared to control TECs (p < 0.001). NK cells treated in vitro with soluble Clr-b and Clr-f proteins reduced their capacity to kill TECs (p < 0.05). Hence, NK cell cytotoxicity can be inhibited by Clr proteins on the surface of TECs. Our study suggests a synergistic effect of Clr molecules in regulating NK cell function in renal cells and this may represent an important endogenous regulatory system to limit NK cell-mediated organ injury during inflammation 2024-01-01T00:00:00Z http://localhost:8080/xmlui/handle/123456789/9219 Title: Cytokine levels in gingival tissues as an indicator to understand periodontal disease severity Authors: Balu, Pratebha; Kumar Balakrishna Pillai, Agiesh; Mariappan, Vignesh; Ramalingam, Sudhakar Abstract: Cytokines regulate periodontal pathogenesis and are relevant estimates of current disease activity. There is sparse information on status of cytokine protein levels in periodontal pocket (gingival) tissues. The current study analysed proteins and transcripts of selected cytokines in varying severity of periodontal disease and elucidated cytokine/cytokine ratios that best indicated periodontal disease severity, in gingival tissues. A total of 92 participants comprising of generalised moderate periodontitis (GMP, n = 18), generalised severe periodontitis (GSP, n = 46) and periodontally healthy controls (PHC, n = 25) were recruited for the study. Interproximal gingival tissue samples were utilised for cytokine protein estimation and mRNA quantification by qRT-PCR and ELISA respectively. Selected key pro and anti-inflammatory cytokines, also representative of various Th subsets were analysed. ROC curve analysis was performed and Youden index was calculated for individual cytokines and pro/ anti-inflammatory cytokine ratio to estimate the best indicator of periodontal severity/progression in tissues. IL- 1β, TGF-β and IFN-γ cytokine protein levels varied significantly (p ≤ 0.05) with severity of periodontal disease between groups. On comparison between deep and shallow sites within same participant, deep sites showed significant elevation of TGF-β (p ≤ 0.01) and IFN-γ (p ≤ 0.05) and IL-17 cytokines and shallow sites showed elevation of IL-4(p ≤ 0.01) and IL-1β (p ≤ 0.05) cytokines. Analysis of transcripts showed IFN-γ and IL-1β transcript predominance in GSP (p = 0.01) compared to PHC. ROC analysis illustrated 97% sensitivity, 93% specificity with Youden index of 90% for IL-1β cytokine and 81%sensitivity, 79% specificity with a Youden index of 60% for IL-1β/TGF-β ratio In periodontal pocket tissue, a lack of distinct predominance of specific cytokines between study groups or between shallow and deep sites affected by periodontal disease was observed. However, ROC analysis of cytokines revealed IL-1β cytokine and IL-1β/TGF-β ratio as promising indicators of periodontal disease severity in gingival tissues. 2024-01-01T00:00:00Z http://localhost:8080/xmlui/handle/123456789/9218 Title: Lymphoblastoid cell lines do not recapitulate physiological circulating B cell subtypes Authors: MacKinnon, Connie; McLean, Ryan; L. Pritchard, Antonia Abstract: Lymphoblastoid cell lines (LCLs) are immortalised peripheral B lymphocytes, transformed via infection with Epstein Barr virus (EBV). The use of LCLs to study B cell function remains controversial and core markers to define physiological B cell populations are not consistent between studies of physiological B cells and LCLs. A consensus on the nature of these commonly used cell lines has not been reached. Recently, a core set of markers to subtype peripheral B cells was proposed, addressing the lack of agreed markers for B cell characterisation. In this present study, the consensus panel was applied to describe the B cell subtypes in LCLs. We found that LCLs were generally not physiologically representative of B cells, with most cells harbouring marker combinations absent on peripheral B cells. Some B cell subtyping markers were fundamentally altered during EBV transformation to LCLs (e.g. CD19, CD21). Notably, most LCLs secreted IgG but the associated marker combinations were predominantly only present in vitro following EBV transformation. This study therefore informs interpretation of past investigations, and planning of future studies using LCLs, as these cells are unlikely to behave like their pre-transformed B cell subtype. 2024-01-01T00:00:00Z http://localhost:8080/xmlui/handle/123456789/9217 Title: Parasitic infections: A new frontier for PGD2 functions Authors: L. Diaz, Bruno; Bandeira-Melo, Christianne Abstract: Prostaglandin (PG)D2 is produced and/or triggered by different parasites to modulate the course of the infection. These findings position PGD2 as a therapeutic target and suggest potential beneficial effects of repositioned drugs that target its synthesis or receptor engagement. However, recent in vivo data may suggest a more nuanced role and warrants further investigation of the role of PGD2 during the full course and complexity of parasitic infections 2024-01-01T00:00:00Z