Priscilla Biswas

Publications (64) View all

• Source

  Available from: microbiologica.net

  Article: Improvement of CXCR3 ligand CXCL11/I-TAC measurement in human plasma and serum.

  Viviana Cremasco, Barbara Mantelli, Adriano Lazzarin, Priscilla Biswas
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  ABSTRACT: The chemokine receptor CXCR3 is involved in cell trafficking dysregulation associated with several inflammatory conditions, including autoimmune and viral diseases. Downregulation of CXCR3, through binding with its ligand CXCL11 (I-TAC), represents a key mechanism in lymphocyte recruitment. Determination of circulating I-TAC can provide useful information in the investigation of inflammatory/infectious conditions. The existing commercial kit does not measure CXCL11/I-TAC in complex matrices, such as human plasma and serum, as reliably as in in vitro-generated cell culture supernatants. We here describe means which lead to an improvement of CXCL11/I-TAC measurement in human plasma and serum.
  The new microbiologica: official journal of the Italian Society for Medical, Odontoiatric, and Clinical Microbiology (SIMMOC) 02/2009; 32(1):125-8. · 1.00 Impact Factor
• Article: In Vivo Treatment with Fusion Inhibitor Enfuvirtide Leads to Increased IL-12 Production by Autologous in Vitro Activated Monocytes from HIV-infected Individuals

  Vecchi Andrea, Hasson Hamid, Galli Andrea, Castagna Antonella, Lazzarin Adriano, Biswas Priscilla
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  ABSTRACT: Enfuvirtide inhibits IL-12 synthesis in vitro . We investigated IL-12 production in monocytes from thirteen chronic, late-stage patients who underwent ENF treatment in vivo for at least 12 weeks. Peripheral blood mononuclear cells from frozen samples and flow cytometry was used. Interestingly, a statistically significant increase of the percentage of IL-12-producing activated monocytes was documented after treatment with the ENF-containing antiretroviral regimen. In about 50% of the subjects the increase of IL-12 coexistedwith increase of CD4 T lymphocyte count and, unexpectedly, serum IgE and with decrease of HIV-1 viremia. Lack of a true association could be due to the retrospective nature and small sample size of our study.Nevertheless, in vitro evaluation of IL-12 production in response to antiretroviral drugs should be taken into consideration as it could reflect the status of at least one arm of innate immunity and complement the information derived solely by the CD4 T lymphocyte count.
  Journal of Antivirals & Antiretrovirals. 01/2009;
• Source

  Available from: Lucinda Furci

  Article: Identification of the platelet-derived chemokine CXCL4/PF-4 as a broad-spectrum HIV-1 inhibitor.

  David J Auerbach, Yin Lin, Huiyi Miao, Raffaello Cimbro, Michelle J Difiore, Monica E Gianolini, Lucinda Furci, Priscilla Biswas, Anthony S Fauci, Paolo Lusso
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  ABSTRACT: The natural history of HIV-1 infection is highly variable in different individuals, spanning from a rapidly progressive course to a long-term asymptomatic infection. A major determinant of the pace of disease progression is the in vivo level of HIV-1 replication, which is regulated by a complex network of cytokines and chemokines expressed by immune and inflammatory cells. The chemokine system is critically involved in the control of HIV-1 replication by virtue of the role played by specific chemokine receptors, most notably CCR5 and CXCR4, as cell-surface coreceptors for HIV-1 entry; hence, the chemokines that naturally bind such coreceptors act as endogenous inhibitors of HIV-1. Here, we show that the CXC chemokine CXCL4 (PF-4), the most abundant protein contained within the α-granules of platelets, is a broad-spectrum inhibitor of HIV-1 infection. Unlike other known HIV-suppressive chemokines, CXCL4 inhibits infection by the majority of primary HIV-1 isolates regardless of their coreceptor-usage phenotype or genetic subtype. Consistent with the lack of viral phenotype specificity, blockade of HIV-1 infection occurs at the level of virus attachment and entry via a unique mechanism that involves direct interaction of CXCL4 with the major viral envelope glycoprotein, gp120. The binding site for CXCL4 was mapped to a region of the gp120 outer domain proximal to the CD4-binding site. The identification of a platelet-derived chemokine as an endogenous antiviral factor may have relevance for the pathogenesis and treatment of HIV-1 infection.
  Proceedings of the National Academy of Sciences 05/2012; 109(24):9569-74. · 9.68 Impact Factor
• Source

  Available from: Priscilla Biswas

  Article: A matter of life and death: more members of the TNF receptor family join human γδ T lymphocytes.

  Priscilla Biswas, Marina Ferrarini
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  ABSTRACT: Vγ9Vδ2 γδ lymphocytes represent a T-cell subset involved in the immune response towards pathogens and tumors. The interesting paper by Barros et al [1], and commented on by Born and O'Brien [2], has shown that these cells constitutively express CD27, a member of the TNF receptor (TNF-R) family, and upregulate its cognate ligand, CD70, upon TCR-engagement by γδ-specific phosphate antigens. The resulting CD70-CD27 interaction promoted proliferation, survival and Th1-cell differentiation, thereby indicating that members of the TNF-R family are critical regulators of γδ T-cell function [1]. The study by Barros et al [1] adds to previous work highlighting a pivotal role for TNF-TNF-R in γδ as compared with the role in αβ lymphocytes [3].
  European Journal of Immunology 12/2011; 42(3):803-4. · 5.10 Impact Factor
• Article: Correction: Rational design of HIV vaccine and microbicides: report of the EUROPRISE annual conference.

  Britta Wahren, Priscilla Biswas, Marie Borggren, Adam Coleman, Kelly Da Costa, Winni De Haes, Tessa Dieltjens, Stefania Dispinseri, Katrijn Grupping, David Hallengard, [......], Paolo Palma, Marc Reudelsterz, Janna Seifried, Philippe Selhorst, Annette Skold, Hannes Uchtenhagen, Marit J van Gils, Caroline Weber, Robin Shattock, Gabriella Scarlatti
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  ABSTRACT: ABSTRACT: Following the publication of this article (Journal of Translational Medicine, 8:72), it was noted that a co-author had been omitted from the authors list. The submitting authors would like to apologise to Hannes Uchtenhagen for this error. The Competing interests and Authors' contributions sections have now been updated to reflect this amendment.
  Journal of Translational Medicine 09/2010; 8(1):82. · 3.41 Impact Factor