Mridu Acharya, PhD

Mridu Acharya, PhD

Research Title: Principal Investigator

Research Center: Center for Immunity and Immunotherapies

  • Biography

    I am a principal investigator at Seattle Children's Research Institute, CIIT. I received my PhD from University of Glasgow, Scotland, UK, in 2008 and then moved to Massachusetts General Hospital/Harvard Medical School for post-doctoral training. In December 2013, I moved to Benaroya Research Institute, Seattle as a Staff Scientist and subsequently became Assistant Member in October 2016 and moved to Seattle Children's Research Institute on Oct 2018.

     

     

    • Related Pages

    • Acharya Lab

      Acharya Lab

      The Acharya lab studies how immune cells integrate signals from pathogens and their environment to produce effective immunity against pathogens while maintaining tolerance to self-derived antigens.

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  • Publications

    Other Publications

    • Raso F, Sagadiev S, Du S, Gage E, Arkatkar T, Metzler G, Stuart LM, Orr MT, Rawlings DJ, Jackson SW, Lacy-Hulbert A, Acharya M
      αv Integrins regulate germinal center B cell responses through noncanonical autophagy.
      29999501 The Journal of clinical investigation, 2018 Aug 31 : 128(9)4163-4178 PMCID:PMC6118577
    • Raso F, Sagadiev S, Du S, Gage E, Arkatkar T, Metzler G, Stuart LM, Orr MT, Rawlings DJ, Jackson SW, Lacy-Hulbert A, Acharya M
      αv Integrins regulate germinal center B cell responses through noncanonical autophagy.
      29999501 The Journal of clinical investigation, 2018 Aug 31 : 128(9)4163-4178 PMCID:PMC6118577
    • Tam JM, Mansour MK, Acharya M, Sokolovska A, Timmons AK, Lacy-Hulbert A, Vyas JM
      The Role of Autophagy-Related Proteins in Candida albicans Infections.
      27043636 Pathogens (Basel, Switzerland), 2016 Mar 29 : 5(2) PMCID:PMC4931385
    • Tam JM, Mansour MK, Acharya M, Sokolovska A, Timmons AK, Lacy-Hulbert A, Vyas JM
      The Role of Autophagy-Related Proteins in Candida albicans Infections.
      27043636 Pathogens (Basel, Switzerland), 2016 Mar 29 : 5(2) PMCID:PMC4931385
    • Acharya M, Sokolovska A, Tam JM, Conway KL, Stefani C, Raso F, Mukhopadhyay S, Feliu M, Paul E, Savill J, Hynes RO, Xavier RJ, Vyas JM, Stuart LM, Lacy-Hulbert A
      αv Integrins combine with LC3 and atg5 to regulate Toll-like receptor signalling in B cells.
      26965188 Nature communications, 2016 Mar 11 : 710917 PMCID:PMC4792966
    • Acharya M, Sokolovska A, Tam JM, Conway KL, Stefani C, Raso F, Mukhopadhyay S, Feliu M, Paul E, Savill J, Hynes RO, Xavier RJ, Vyas JM, Stuart LM, Lacy-Hulbert A
      αv Integrins combine with LC3 and atg5 to regulate Toll-like receptor signalling in B cells.
      26965188 Nature communications, 2016 Mar 11 : 710917 PMCID:PMC4792966
    • Tam JM, Mansour MK, Khan NS, Seward M, Puranam S, Tanne A, Sokolovska A, Becker CE, Acharya M, Baird MA, Choi AM, Davidson MW, Segal BH, Lacy-Hulbert A, Stuart LM, Xavier RJ, Vyas JM
      Dectin-1-dependent LC3 recruitment to phagosomes enhances fungicidal activity in macrophages.
      24842831 The Journal of infectious diseases, 2014 Dec 1 : 210(11)1844-54 PMCID:PMC4271056
    • Tam JM, Mansour MK, Khan NS, Seward M, Puranam S, Tanne A, Sokolovska A, Becker CE, Acharya M, Baird MA, Choi AM, Davidson MW, Segal BH, Lacy-Hulbert A, Stuart LM, Xavier RJ, Vyas JM
      Dectin-1-dependent LC3 recruitment to phagosomes enhances fungicidal activity in macrophages.
      24842831 The Journal of infectious diseases, 2014 Dec 1 : 210(11)1844-54 PMCID:PMC4271056
    • Overstreet MG, Gaylo A, Angermann BR, Hughson A, Hyun YM, Lambert K, Acharya M, Billroth-Maclurg AC, Rosenberg AF, Topham DJ, Yagita H, Kim M, Lacy-Hulbert A, Meier-Schellersheim M, Fowell DJ
      Inflammation-induced interstitial migration of effector CD4⁺ T cells is dependent on integrin αV.
      23933892 Nature immunology, 2013 Sept. : 14(9)949-58 PMCID:PMC4159184
    • Overstreet MG, Gaylo A, Angermann BR, Hughson A, Hyun YM, Lambert K, Acharya M, Billroth-Maclurg AC, Rosenberg AF, Topham DJ, Yagita H, Kim M, Lacy-Hulbert A, Meier-Schellersheim M, Fowell DJ
      Inflammation-induced interstitial migration of effector CD4⁺ T cells is dependent on integrin αV.
      23933892 Nature immunology, 2013 Sept. : 14(9)949-58 PMCID:PMC4159184
    • Edkins AL, Borland G, Acharya M, Cogdell RJ, Ozanne BW, Cushley W
      Differential regulation of monocyte cytokine release by αV and β(2) integrins that bind CD23.
      22348662 Immunology, 2012 June : 136(2)241-51 PMCID:PMC4489923
    • Acharya M, Mukhopadhyay S, Païdassi H, Jamil T, Chow C, Kissler S, Stuart LM, Hynes RO, Lacy-Hulbert A
      αv Integrin expression by DCs is required for Th17 cell differentiation and development of experimental autoimmune encephalomyelitis in mice.
      21099114 The Journal of clinical investigation, 2010 Dec. : 120(12)4445-52 PMCID:PMC2993596
    • Païdassi H, Acharya M, Lacy-Hulbert A
      Alpha (v) integrins license regulatory T cells to apoptotic cells and self-associated antigens.
      20958318 Annals of the New York Academy of Sciences, 2010 Oct. : 120968-76

Overview

Research Description

Antigen binding to immune cells activates a complex network of receptors depending on the type of the antigen and other micro-environmental signals. These initial interactions determine the type of immune response that is subsequently generated. My research interest is in understanding how signals from different types of immune receptors and cytoskeletal molecules are integrated to produce an immune response tailored to the type of antigen encountered. B-lymphocytes provide an excellent model to study these kinds of signals because their stages of development and functional specialization during various types of immune responses have been well illustrated. Understanding how these early mechanistic events regulate recognition and processing of antigens would allow us to develop novel strategies to enhance B cell activation to antigens in vaccines, while preventing activation by self-antigens during autoimmunity.

Currently we are using a combination of cell biology, mouse models, human immunology and gene-editing to study how B-lymphocytes integrate signals from antigens and their environment to produce effective responses to pathogens while maintaining tolerance to self-derived antigens.

Expansion of antigen-specific B cells during immune response to viruses

We are investigating how novel proteins and pathways such as integrin signaling and autophagy proteins impact expansion of germinal center B cells, memory B cells, long-lived plasma cells and affinity maturation of antibodies during immune response to influenza virus.

Molecular mechanisms of intracellular trafficking during B cell activation

We are using a combination of microscopy, biochemistry and gene editing techniques to understand signaling and intracellular trafficking of: (a) cytoskeletal receptors such as integrins, (b) immune receptors such as B cell receptor , toll-like receptors and (c) molecules such as kinases and autophagy proteins during B cell stimulation by various types of ligands and antigens.

B cell activation during human autoimmune diseases

In collaboration with researchers at Benaroya Research Institute, using bio-repository human samples we are studying B cell activation during SLE to identify early events that lead to activation of self-reactive B cells during autoimmune diseases. Similarly using these samples, we are also studying the role of genetic variants in cytoskeletal proteins and autophagy pathway to identify novel targets that can modify B cell activation during autoimmune diseases.

 

Research Focus Area

Autoimmunity, Vaccines