We examined the importance of T cell-independent B cell activity in the resolution of primary murine (EDIM) rotavirus infection in adult mice. We showed that Rag 1 (C57BL / 6 background) and Rag 2 (BALB / c background) knockout mice, which lack both T and B cells, chronically shed high levels of rotavirus Ag in stool samples following oral inoculation. However, nude mice (BALB / c and C57BL / 6 backgrounds) and alpha beta TCR knockout mice (C57BL / 6 background) chronically shed 100-fold lower levels of virus in stool samples. Thus, B cells appeared to sharply reduce the level of chronic rotavirus shedding by a T cell-independent mechanism. C57BL / 6 mice depleted of CD4(+) cells or both CD4(+) and CD8(+) cells were also unable to resolve primary rotavirus infection but chronically shed equally low levels of rotavirus Ag in stool samples, whereas mice depleted of only CD8(+) cells resolved infection. Similar results were obtained with a second rotavirus strain (EC(w)) in which virus was shed chronically in stool samples at low levels in alpha beta TCR knockout mice and at high levels in Rag 1 knockout mice. Virus-specific intestinal IgA was readily detected in mice lacking thymic T cells and alpha beta T cells and in mice depleted of CD4(+) cells but levels were 95 % reduced in comparison to immunocompetent control mice. Together, these results show that B cells lacking CD4(+) T cell help have the capacity to substantially reduce rotavirus shedding, possibly through the production of T cell-independent IgA to rotavirus, but full resolution requires alpha beta T cells.
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http://dx.doi.org/10.1002/1521-4141(200111)31:11<3380::aid-immu3380>3.0.co;2-0 | DOI Listing |
Clin Transl Med
January 2025
Vascular Research Laboratory, IIS-Fundación Jiménez Díaz, Madrid, Spain.
Background: Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipids and leukocytes within the arterial wall. By studying the aortic transcriptome of atherosclerosis-prone apolipoprotein E (ApoE) mice, we aimed to identify novel players in the progression of atherosclerosis.
Methods: RNA-Seq analysis was performed on aortas from ApoE and wild-type mice.
Elife
January 2025
Department of Neurology, Weill Institute for Neuroscience, University of California San Francisco, San Francisco, United States.
Mutations in Sonic Hedgehog (SHH) signaling pathway genes, for example, (SUFU), drive granule neuron precursors (GNP) to form medulloblastomas (MB). However, how different molecular lesions in the Shh pathway drive transformation is frequently unclear, and mutations in the cerebellum seem distinct. In this study, we show that fibroblast growth factor 5 (FGF5) signaling is integral for many infantile MB cases and that expression is uniquely upregulated in infantile MB tumors.
View Article and Find Full Text PDFFASEB J
January 2025
August Krogh Section for Human and Molecular Physiology, Department of Nutrition, Exercise and Sports, University of Copenhagen, Copenhagen, Denmark.
The kinases AMPK, and mTOR as part of either mTORC1 or mTORC2, are major orchestrators of cellular growth and metabolism. Phosphorylation of mTOR Ser1261 is reportedly stimulated by both insulin and AMPK activation and a regulator of both mTORC1 and mTORC2 activity. Intrigued by the possibilities that Ser1261 might be a convergence point between insulin and AMPK signaling in skeletal muscle, we investigated the regulation and function of this site using a combination of human exercise, transgenic mouse, and cell culture models.
View Article and Find Full Text PDFJ Cereb Blood Flow Metab
January 2025
Multidisciplinary Brain Protection Program (MBPP), Department of Anesthesiology, Duke University Medical Center, Durham, NC, USA.
Cardiac arrest (CA) is a life-threatening condition that requires immediate medical attention. Considerable advances in resuscitation have led to an increasing number of patients who survive the initial arrest event. However, among this growing patient population, morbidity and mortality rates remain strikingly high.
View Article and Find Full Text PDFChin Med J Pulm Crit Care Med
December 2024
Department of Respiratory Medicine, National Key Clinical Specialty, Branch of National Clinical Research Center for Respiratory Disease, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China.
Background: Glucocorticoid-induced transcript 1 (GLCCI1) has been reported to be associated with the efficiency of inhaled glucocorticoids in patients with asthma. This study aimed to investigate the role of GLCCI1 in the regulation of nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) family pyrin domain-containing 3 (NLRP3) by the phosphatidylinositol 3-kinase (PI3K) pathway in the pathogenesis of allergic asthma.
Methods: The expression levels of genes encoding GLCCI1, NLRP3 inflammasome components, and PI3K pathway-related indicators were detected in cells isolated from induced sputum from patients with asthma and healthy controls.
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