Laura Mandik-Nayak, PhD

Photo of Laura Mandik-Nayak


Phone: 484.476.8427

Fax: 610.645.8533

Office: R130

Department: Faculty

Association: Resident Faculty

Research Interests

  • Autoimmune diseases, including rheumatoid arthritis, systemic lupus erythematosus, and type I diabetes. Determining factors that lead to the initiation and progression of the joint-specific autoimmune response in individuals with rheumatoid arthritis.
  • Google Scholar page

About her work

Dr. Mandik-Nayak is working to determine the factors that lead to the development and progression of the joint-specific autoimmune response found in those with rheumatoid arthritis

Awards and Honors

  • Gina Finzi Memorial Student Fellowship Award, Lupus Foundation of America (1994)
  • Dr. Monica H.M. Shander Fellowship Award, The Wistar Institute (1997-1998)
  • Saul Winegrad Award for Outstanding Dissertation, University of Pennsylvania (1998)
  • Junior Faculty Travel Award, American Association of Immunologists (2010)
  • Laboratory Travel Award, American Association of Immunologists (2014)

Current Appointments

  • 2013 to Present: Associate Professor, Lankenau Institute for Medical Research
  • 2009 to Present: Adjunct Assistant Professor, Dept. of Pathology and Laboratory Medicine, Drexel University College of Medicine, Philadelphia
  • 2008 to Present: Assistant Professor, Dept. of Microbiology and Immunology, Jefferson Medical College, Thomas Jefferson University, Philadelphia
  • 2006 to 2013: Assistant Professor, Lankenau Institute for Medical Research


  • BS, Biology, Bucknell University, Lewisburg, PA, 1993
  • PhD, Immunology, University of Pennsylvania, Philadelphia, PA, 1999
  • Postdoctoral Fellowship, Washington University, 1999-2000


Rheumatoid arthritis (RA) is an autoimmune disease that affects approximately 1.3 million individuals in the United States. Of those, about 75 percent are women.

RA is a chronic (i.e., long-term) disease that causes pain, stiffness, swelling, and limited motion and function of many joints. While the cause of RA is unknown, new research is helping to shed light on what makes the immune system attack the body and create the joint inflammation that plagues patients with RA. We know that immune cells (T and B cells) play critical roles in the disease’s progression.

RA eventually leads to debilitating destruction of cartilage and bone, and unfortunately there is no cure. Treatments to manage symptoms have improved greatly over the years. However, they are ineffective at controlling disease progression, as they rely on the reduction of inflammation by focusing only on the end stage of the disease.

Focus on RA triggers

Dr. Laura Mandik-Nayak is taking a different approach by targeting the early stage of RA. Her lab focuses on the triggering mechanisms by which the immune system becomes activated to induce inflammation in the joints.

Recently, Dr. Mandik-Nayak identified a pathway that triggers the activation of autoreactive T and B cells during the development of arthritis. This pathway involves an enzyme implicated in immune regulation, IDO (indoleamine 2,3-dioxygenase). IDO activity is elevated in arthritis patients. Dr. Mandik-Nayak’s recent data demonstrate that inhibiting IDO activity interferes with immune cell activation and arthritis development, suggesting that the IDO pathway is an important mediator of the disease process.

Her group examined both IDO1 and IDO2 in relation to autoimmune arthritis development. Their work reveals that IDO2, but not IDO1, is an important component of developing arthritis symptoms. They found that IDO2 drives the autoreactive T and B cell response leading to arthritis. The enzyme appears to specifically affect the production of autoantibodies, but does not seem to play a role in mediating antibody responses in general.

Dr. Mandik-Nayak is investigating if using an IDO inhibitor could lead to a therapeutic agent for RA. Her work may lead to a new approach and to novel medicines for the prevention and treatment of RA and possibly other autoimmune diseases.

About her lab

Since starting the first immunological laboratory at LIMR in 2006, Dr. Mandik-Nayak has focused on mediators that drive the inflammatory autoimmune response in mouse models of RA, systemic lupus erythematosus, and rheumatoid heart disease, with an emphasis not only on the immunoregulatory enzymes of IDO, but also the small GTPase RhoB.

Lab personnel

  • Lauren Merlo, PhD, Research Assistant Professor
  • Samantha Grabler, BS, Biomedical Research Assistant

Selected publications

IDO2 in Immunomodulation and Autoimmune Disease. Prendergast GC, Metz R, Muller AJ, Merlo LM, Mandik-Nayak L. Front Immunol. 2014 Nov 20;5:585.

1-Methyl-tryptophan synergizes with methotrexate to alleviate arthritis in a mouse model of arthritis. Pigott E, DuHadaway JB, Muller AJ, Gilmour S, Prendergast GC, Mandik-Nayak L. Autoimmunity. 2014 Sep;47(6):409-18.

Addition of indoleamine 2,3-dioxygenase inhibitor to B cell-depletion therapy blocks autoreactive B cell activation and recurrence of arthritis in K/BxN mice. Pigott, E, Mandik-Nayak, L Arthritis Rheum. 2012 64:2169-2178.

IDO2 is a critical mediator of autoantibody production and inflammatory pathogenesis in a mouse model of autoimmune arthritis. Merlo LM, Pigott E, DuHadaway JB, Grabler S, Metz R, Prendergast GC, Mandik-Nayak L. J Immunol. 2014 Mar 1;192(5):2082-90.

IDO2 is critical for IDO1-mediated T-cell regulation and exerts a non-redundant function in inflammation. Metz R, Smith C, DuHadaway JB, Chandler P, Baban B, Merlo LM, Pigott E, Keough MP, Rust S, Mellor AL, Mandik-Nayak L, Muller AJ, Prendergast GC. Int Immunol. 2014 Jul;26(7):357-67.

IDO2 Modulates T Cell-Dependent Autoimmune Responses through a B Cell-Intrinsic Mechanism. Merlo LM, DuHadaway JB, Grabler S, Prendergast GC, Muller AJ, Mandik-Nayak L. J Immunol. 2016 Jun 1;196(11):4487-97.

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