The expression of allograft inflammatory factor-1 (AIF-1) in 2,4,6-trinitrobenzene sulphonic acid (TNBS)-induced colitis, a model for T helper 1 (Th1) type disease, was investigated in BALB/c mice. The AIF-1 expression was significantly increased in the colitis lesion compared to that in the normal colon. We then prepared AIF-1 transgenic mice (Tgm) with the BALB/c background that express high levels of AIF-1 in lymphoid tissues and the colon. When AIF-1 Tgm were administrated TNBS, the TNBS-induced colitis was ameliorated compared with that in non-transgenic littermates. The amelioration of colitis was associated with the low expression of interleukin-1beta in the colon. The present findings suggest that AIF-1 regulates Th1-type inflammatory responses.
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http://dx.doi.org/10.1046/j.1365-2567.2003.01714.x | DOI Listing |
Nat Cardiovasc Res
January 2025
Department of Pathology, Northwestern University, Chicago, IL, USA.
Myocardial infarction (MI) mobilizes macrophages, the central protagonists of tissue repair in the infarcted heart. Although necessary for repair, macrophages also contribute to adverse remodeling and progression to heart failure. In this context, specific targeting of inflammatory macrophage activation may attenuate maladaptive responses and enhance cardiac repair.
View Article and Find Full Text PDFAm J Transplant
December 2024
The Dumont-UCLA Transplantation Center, Department of Surgery, Division of Liver and Pancreas Transplantation, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095; Department of Surgery, Medical University of South Carolina, Charleston, SC 29425. Electronic address:
As important immune regulatory cells, whether innate lymphoid cells (ILCs) are involved in liver transplantation (LT) remains unclear. In a murine orthotopic LT model, we dissected roles of ILCs in liver ischemia-reperfusion injury (IRI). Wild type (WT) grafts suffered significantly higher IRI in Rag2-γc double knockout (DKO) than Rag2 KO recipients, in association with downregulation of group 1 ILCs genes, including IFN-γ.
View Article and Find Full Text PDFWorld J Stem Cells
December 2024
Department of Ultrasonic, The First People's Hospital of Yunnan Province, Kunming 650032, Yunnan Province, China.
Background: Heart transplantation is a crucial intervention for severe heart failure, yet the challenge of organ rejection is significant. Bone marrow mesenchymal stem cells (BMSCs) and their exosomes have demonstrated potential in modulating T cells, dendtitic cells (DCs), and cytokines to achieve immunomodulatory effects. DCs, as key antigen-presenting cells, play a critical role in shaping immune responses by influencing T-cell activation and cytokine production.
View Article and Find Full Text PDFTranspl Int
December 2024
Department of Pathology, Necker-Enfants Malades Hospital, Assistance Publique-Hopitaux de Paris, Paris, France.
While the Banff classification dichotomizes kidney allograft rejection based on the localization of the cells in the different compartments of the cortical kidney tissue [schematically interstitium for T cell mediated rejection (TCMR) and glomerular and peritubular capillaries for antibody-mediated rejection (AMR)], there is a growing evidences that subtyping the immune cells can help refine prognosis prediction and treatment tailoring, based on a better understanding of the pathophysiology of kidney allograft rejection. In the last few years, multiplex IF techniques and automatic counting systems as well as transcriptomics studies (bulk, single-cell and spatial techniques) have provided invaluable clues to further decipher the complex puzzle of rejection. In this review, we aim to better describe the inflammatory infiltrates that occur during the course of kidney transplant rejection (active AMR, chronic active AMR and acute and chronic active TCMR).
View Article and Find Full Text PDFKidney transplantation (KT) is the treatment of choice for chronic kidney disease (CKD) patients, but there is a continued loss of grafts in the long-term (50% at 10 years) due to either patient 's death or chronic allograft dysfunction. Metabolic syndrome (MS) is very prevalent after KT (30-40%) and its components contribute to the appearance of non-alcoholic fatty liver disease/metabolic dysfunction-associated fatty liver disease (NAFLD/MAFLD) and non-alcoholic steatohepatitis (NASH), which represents the hepatic component of MS. Furthermore, about 20-40% of KT recipients present early graft inflammation, including subclinical inflammation.
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