The study on mice with experimental generalized Klebsiella infection, carried out with the use of microbiologic, immunologic and pathomorphologic methods, revealed that the intraperitoneal injection of type I interferon into the animals prevented their death and led to the rapid elimination of the infective agent from their body, enhanced the phagocytic and metabolic activity of polymorphonuclear lymphocytes of their peritoneal exudate, decreased the manifestation of microcirculatory and dystrophic changes in the parenchyma of their internal organs.
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Gut TLRs and IFN pathway mRNA expression and frequencies of CD4 T Cell expressing CD38 or HLA-DR go in Parallel During HIV Immunopathogenesis.
Immunol Lett
January 2025
Department of Public Health and Infectious Diseases, Sapienza University of Rome, Italy. Electronic address:
Whereas much knowledge exists on the expression of IFN pathways in the blood of people living with HIV (PLWH), its role has only recently been appreciated in the gastrointestinal tract. Thus, the aim was to evaluate the gut mRNA expression levels of innate immune genes involved in the HIV-host interaction and their association with CD4 T cell activation in long-term HAART-experienced PLWH. PLWH had increased TLR4, IFN-α2, IFN-α14, IFN-β and IFNAR1 mRNAs levels in LPLs, as well as increased frequencies of CD4 T lymphocytes expressing CD38 or HLA-DR compared to the healthy donors.
View Article and Find Full Text PDFTargeting SETDB1 in cancer and immune regulation: Potential therapeutic strategies in cancer.
Kaohsiung J Med Sci
January 2025
Department of Pathology, Duke University Medical Center, Durham, North Carolina, USA.
SET domain bifurcated histone lysine methyltransferase 1 (SETDB1/ESET), a pivotal H3K9 methyltransferase, has been extensively studied since its discovery over two decades ago. SETDB1 plays critical roles in immune regulation, including B cell maturation, T-cell activity modulation, and endogenous retrovirus (ERV) silencing. While essential for normal immune cell function, SETDB1 overexpression in cancer cells disrupts immune responses by suppressing tumor immunogenicity and facilitating immune evasion.
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