{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nThe two studies explore the wide‐ranging effects of interferon gamma (IFNγ) in inflammatory conditions, highlighting its critical involvement in central nervous system demyelination and vascular inflammation. In one study examining an experimental autoimmune encephalomyelitis model combined with cuprizone toxicity, loss of IFNγ receptor signaling delayed demyelination while promoting rapid remyelination. These findings emphasize IFNγ’s role in modulating immune cell recruitment and oligodendrocyte precursor cell mobilization in demyelinating disorders."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n"}, {"type": "p", "children": [{"type": "t", "text": "\nThe second study focused on atherosclerosis, a chronic lipid-driven inflammatory disease, revealing that IFNγ signaling in macrophages plays a pro-atherosclerotic role. By dissecting the cell-specific effects of IFNγ, the research underscores the cytokine’s capacity to enhance inflammatory responses within the arterial wall, further implicating it as a critical mediator in vascular pathology."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n"}, {"type": "p", "children": [{"type": "t", "text": "\nNotably, neither study specifically addresses the function of PRAMEF22. Although the abstracts provide valuable insights into IFNγ-mediated immune modulation in demyelination, remyelination, and atherosclerosis, they do not mention or elucidate any role for PRAMEF22. As such, the function of PRAMEF22 in these inflammatory contexts remains undefined in these reports, underscoring the need for future studies to determine whether it might interact with or influence IFNγ signaling and related cellular processes.\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Paula Maña, David Liñares, Sue Fordham, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Deleterious role of IFNgamma in a toxic model of central nervous system demyelination."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Am J Pathol (2006)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.2353/ajpath.2006.050799"}], "href": "https://doi.org/10.2353/ajpath.2006.050799"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "16651614"}], "href": "https://pubmed.ncbi.nlm.nih.gov/16651614"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Marieke C S Boshuizen, Annette E Neele, Marion J J Gijbels, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Myeloid interferon-γ receptor deficiency does not affect atherosclerosis in LDLR(-/-) mice."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Atherosclerosis (2016)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.atherosclerosis.2016.01.026"}], "href": "https://doi.org/10.1016/j.atherosclerosis.2016.01.026"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "26828750"}], "href": "https://pubmed.ncbi.nlm.nih.gov/26828750"}]}]}]}