The ability of normal, parental type T cells to initiate an immune response and to generate memory T cells in T-cell deficient F1 mice was investigated using two types of F1 recipients: Congenitally athymic (nude) mice and thymectomized, lethally irradiated, syngeneic bone marrow reconstituted (TIR) mice. In contrast to normal syngeneic T cells, normal parental type T cells elicited neither immune response nor memory T cells in F1 T-cell deficient mice. Parental T cells were ineffective even when obtained from chimeric donors tolerant to the second parental type transplantation antigens and normal, parental T cells did not counteract the restorative activity of F1 T cells in F1 T-cell-deficient recipients. These two latter findings exclude a suppression due to an ongoing GVH reaction as a possible cause for failure of parental T cells to restore F1 T-cell-deficient mice.
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http://dx.doi.org/10.3109/08820138209057744 | DOI Listing |
Proc Natl Acad Sci U S A
January 2025
Centre for Tuberculosis Research, Tuberculosis Research Laboratory, Translational Health Science and Technology Institute, National Capital Region Biotech Science Cluster 3rd Milestone, Faridabad, Haryana 121001, India.
Itaconate, an abundant metabolite produced by macrophages upon interferon-γ stimulation, possesses both antibacterial and immunomodulatory properties. Despite its crucial role in immunity and antimicrobial control, its mechanism of action and dissimilation are poorly understood. Here, we demonstrate that infection of mice with increases itaconate levels in lung tissues.
View Article and Find Full Text PDFAdv Sci (Weinh)
January 2025
Institute of Biomedicine and Translational Medicine, University of Tartu, Ravila 14B, Tartu, 50411, Estonia.
In triple-negative breast cancer (TNBC), pro-tumoral macrophages promote metastasis and suppress the immune response. To target these cells, a previously identified CD206 (mannose receptor)-binding peptide, mUNO was engineered to enhance its affinity and proteolytic stability. The new rationally designed peptide, MACTIDE, includes a trypsin inhibitor loop, from the Sunflower Trypsin Inhibitor-I.
View Article and Find Full Text PDFFront Pediatr
January 2025
Pathology Department, Anhui Provincial Children's Hospital, Hefei, Anhui, China.
Introduction: Cryptorchidism can damage cells in the cryptorchid testes due to elevated local temperatures, potentially impacting the fertility of the child in adulthood. Research indicates that vitamin D enhances sperm quality in adult males. This study aimed to explore whether vitamin D inhibits NLRP3 activation, thus helping to mitigate heat stress damage to testicular spermatogenic and Sertoli cells.
View Article and Find Full Text PDFSci Rep
January 2025
Reproductive Medicine Center, Jiangxi Maternal and Child Health Hospital, 318 Bayi Avenue, Nanchang, 330006, China.
To explore the genetic cause of a four-generation severe intellectual disability in a Chinese family using nanopore sequencing and to provide genetic counseling and reproductive guidance for family members. Multiple genetic analyses of the proband and family members were performed, including chromosome karyotype analysis, whole exome sequencing, nanopore sequencing, PCR amplification, and Sanger sequencing. The results of G-binding karyotyping, CGG repeats for FMR1, GGC repeats for NOTCH2NCL, and trio-whole-exome sequencing were negative for the proband and his parents.
View Article and Find Full Text PDFBiomedica
December 2024
Servicio de Inmunología y Alergología, Fundación Universitaria Ciencias de la Salud - FUCS, Bogotá, D. C., Colombia.
Cernunnos/XLF deficiency is a rare, severe combined immunodeficiency, inherited in an autosomal recessive pattern (OMIM number: 611290), related to the NHEJ1 gene. This gene participates in the DNA non-homologous end-joining pathway, repairing double-strand breaks in the DNA of mammalian cells. The clinical features include growth retardation, microcephaly, triangle-shaped face, recurrent infections, fibroblast's excessive sensitivity to gamma-ionizing radiation, and hypogammaglobulinemia; also, low counts of subpopulations of B and T lymphocytes, with normal values of natural-killer cells.
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