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  <channel rdf:about="https://dspace.nii.res.in//https://dspace.nii.res.in/handle/123456789/44">
    <title>DSpace Community: Principal Investigator- Dr. Vineeta Bal</title>
    <link>https://dspace.nii.res.in//https://dspace.nii.res.in/handle/123456789/44</link>
    <description>Principal Investigator- Dr. Vineeta Bal</description>
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        <rdf:li rdf:resource="https://dspace.nii.res.in//https://dspace.nii.res.in/handle/123456789/1472" />
        <rdf:li rdf:resource="https://dspace.nii.res.in//https://dspace.nii.res.in/handle/123456789/1471" />
        <rdf:li rdf:resource="https://dspace.nii.res.in//https://dspace.nii.res.in/handle/123456789/1421" />
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    </items>
    <dc:date>2026-04-27T15:41:14Z</dc:date>
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  <item rdf:about="https://dspace.nii.res.in//https://dspace.nii.res.in/handle/123456789/1472">
    <title>An efficient immunoassay for the B cell help function of SARS-CoV-2-specific memory CD4+ T cells</title>
    <link>https://dspace.nii.res.in//https://dspace.nii.res.in/handle/123456789/1472</link>
    <description>Title: An efficient immunoassay for the B cell help function of SARS-CoV-2-specific memory CD4+ T cells
Authors: Asgar Ansari, Asgar; Sachan, Shilpa; Jit, Bimal Prasad; Sharma, Ashok; Coshic, Poonam; Sette, Alessandro; Weiskopf, Daniela; Gupta, Nimesh
Abstract: B cell help; B cell survival; Mycobacterium tuberculosis; SARS-CoV-2; SCGF/CLEC11A; T-B cocultures; correlates of protection.</description>
    <dc:date>2022-01-01T00:00:00Z</dc:date>
  </item>
  <item rdf:about="https://dspace.nii.res.in//https://dspace.nii.res.in/handle/123456789/1471">
    <title>Amoxicillin impact on pathophysiology induced by short term high salt diet in mice</title>
    <link>https://dspace.nii.res.in//https://dspace.nii.res.in/handle/123456789/1471</link>
    <description>Title: Amoxicillin impact on pathophysiology induced by short term high salt diet in mice
Authors: Kumar, Suresh; Perumal, Nagarajan; Yadav, P K; Pandey, Ramendra Pati; Chang, Chung-Ming; Raj, V Samuel
Abstract: Current evidence emerging from both human and animal models confirms that high-salt diet consumption over a period modulates the gut ecology and subsequently accelerates the development of the pathophysiology of many metabolic diseases. The knowledge of short-term intake of a high-salt diet (HSD) on gut microbiota and their role in the progression of metabolic pathogenesis and the consequence of a typical course of common antibiotics in this condition has yet not been investigated. The present study elicited this knowledge gap by studying how the gut microbiota profile changes in mice receiving HSD for a short period followed by Amoxicillin treatment on these mice in the last week to mimic a typical treatment course of antibiotics. In this study, we provided a standard chow diet (CD) and HSD for 3 weeks, and a subset of these mice on both diets received antibiotic therapy with Amoxicillin in the 3rd week. We measured the body weight of mice for 3 weeks. After 21 days, all animals were euthanised and subjected to a thorough examination for haemato-biochemical, histopathological, and 16S rRNA sequencing, followed by bioinformatics analysis to determine any changes in gut microbiota ecology. HSD exposure in mice for short duration even leads to a significant difference in the gut ecology with enrichment of specific gut microbiota crucially linked to developing the pathophysiological features of metabolic disease-related inflammation. In addition, HSD treatment showed a negative impact on haemato-biochemical parameters. However, Amoxicillin treatment in HSD-fed mice restored the blood-biochemical markers near to control values and reshaped gut microbiota known for improving the pathophysiological attributes of metabolic disease related inflammation. This study also observed minimal and insignificant pathological changes in the heart, liver, and kidney in HSD-fed mice.</description>
    <dc:date>2022-01-01T00:00:00Z</dc:date>
  </item>
  <item rdf:about="https://dspace.nii.res.in//https://dspace.nii.res.in/handle/123456789/1421">
    <title>Effector/memory CD4 T cells making either Th1 or Th2 cytokines commonly co-express T-bet and GATA-3</title>
    <link>https://dspace.nii.res.in//https://dspace.nii.res.in/handle/123456789/1421</link>
    <description>Title: Effector/memory CD4 T cells making either Th1 or Th2 cytokines commonly co-express T-bet and GATA-3
Authors: Bal, Vineeta; Rath, Satyajit; George, Anna; Das, Arundhoti; Ranganathan, Vidya; Umar, Danish; Thukral, Shipra
Abstract: Naïve CD4 T (NCD4T) cells post-activation undergo programming for inducible production of cytokines leading to generation of memory cells with various functions. Based on cytokine based polarization of NCD4T cells in vitro, programming for either 'Th1' (interferon-gamma [IFNg]) or 'Th2' (interleukin [IL]-4/5/13) cytokines is thought to occur via mutually exclusive expression and functioning of T-bet or GATA-3 transcription factors (TFs). However, we show that a high proportion of mouse and human memory-phenotype CD4 T (MCD4T) cells generated in vivo which expressed either Th1 or Th2 cytokines commonly co-expressed T-bet and GATA-3. While T-bet levels did not differ between IFNg-expressing and IL-4/5/13-expressing MCD4T cells, GATA-3 levels were higher in the latter. These observations were also confirmed in MCD4T cells from FVB/NJ or aged C57BL/6 or IFNg-deficient mice. While MCD4T cells from these strains showed greater Th2 commitment than those from young C57BL/6 mice, pattern of co-expression of TF was similar. Effector T cells generated in vivo following immunization also showed TF co-expression in Th1 or Th2 cytokine producing cells. We speculated that the difference in TF expression pattern of MCD4T cells generated in vivo and those generated in cytokine polarized cultures in vitro could be due to relative absence of polarizing conditions during activation in vivo. We tested this by NCD4T cell activation in non-polarizing conditions in vitro. Anti-CD3 and anti-CD28-mediated priming of polyclonal NCD4T cells in vitro without polarizing milieu generated cells that expressed either IFNg or IL-4/5/13 but not both, yet both IFNg- and IL-4/5/13-expressing cells showed upregulation of both TFs. We also tested monoclonal T cell populations activated in non-polarizing conditions. TCR-transgenic NCD4T cells primed in vitro by cognate peptide in non-polarizing conditions which expressed either IFNg or IL-4/5/13 also showed a high proportion of cells co-expressing TFs, and their cytokine commitment varied depending on genetic background or priming conditions, without altering pattern of TF co-expression. Thus, the model of mutually antagonistic differentiation programs driven by mutually exclusively expressed T-bet or GATA-3 does not completely explain natural CD4 T cell priming outcomes.</description>
    <dc:date>2017-01-01T00:00:00Z</dc:date>
  </item>
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