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John E Harris MD, PhD

TitleAssociate Professor
InstitutionUniversity of Massachusetts Medical School
DepartmentDermatology
AddressUniversity of Massachusetts Medical School
55 Lake Avenue North
Worcester MA 01655
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    Other Positions
    InstitutionUMMS - School of Medicine
    DepartmentDermatology

    InstitutionUMMS - Graduate School of Biomedical Sciences
    DepartmentImmunology and Virology

    InstitutionUMMS - Graduate School of Biomedical Sciences
    DepartmentInterdisciplinary Graduate Program

    InstitutionUMMS - Graduate School of Biomedical Sciences
    DepartmentMD/PhD Program


    Collapse Biography 
    Collapse education and training
    Gordon College, Wenham, MA, United StatesBSPremedicine
    University of Massachusetts Medical School, Worcester, MA, United StatesMD
    University of Massachusetts Medical School, Worcester, MA, United StatesPHDMolecular Medicine

    Collapse Overview 
    Collapse overview


    Investigating contributions of both melanocytes and immune cells to vitiligo



    John HarrisThe goal of my laboratory is to better understand what causes vitiligo in order to develop new treatments.



    Vitiligo is an autoimmune disease that results in the appearance of white spots on the skin. It affects 0.5-2% of the population (about 1/100 people) regardless of race and gender, and can be psychologically devastating for patients due to its disfiguring appearance. The white spots are due to the destruction of melanocytes by T cells. As a physician-scientist, I treat patients with vitiligo and also manage a laboratory that is focused on studying the disease.



    In the lab, we focus on two aspects of vitiligo:



    VIT HandsFirst, we study how abnormal, “stressed” melanocytes alert the immune system to their presence. We believe that, once stressed, melanocytes produce signals that recruit T cells to the skin, which then find the melanocytes and kill them.



    Second, we study how the T cells detect these signals, enter the skin, find the melanocytes, and kill them.



    We use four major systems to answer these questions:





    First, we use a mouse model of vitiligo that we developed, where the mice get spots of vitiligo on their ears, tails, feet and noses. Examining these mice from many angles, their disease looks very much like human vitiligo. The benefit of this system is the powerful tools available to study diseases in mice.

    Second, we are developing humanized mouse models of vitiligo, where we transfer human T cells, or both T cells and skin, from vitiligo patients to immunosuppressed mice that permit the growth of human tissues. The benefit of this system is the ability to study human T cells and skin, and it has the potential to test new treatments on human tissues before attempting clinical trials.

    Third, since I manage a specialty clinic in vitiligo, I regularly collect skin and blood from willing donors to study these processes directly. The benefit of this approach is that we can study the key cells that participate in vitiligo directly from patients, without variables that may change them, including their transfer into mice.

    Fourth, we are conducting a clinical trial to test an investigational new drug as a treatment for vitiligo.



    Using these systems, we have identified one of the critical pathways used by T cells to crawl into the skin and find melanocytes. The first signal in the pathway is IFN-g, a protein made by immune cells, which acts as a powerful master switch to turn on immune responses. IFN-g then turns on CXCL10, which is required for the ability of T cells to find melanocytes and kill them. Imagine an ant that has found a new piece of food on the ground. The ant then lays a chemical trail that others follow to the food. CXCL10 acts like that chemical trail, promoting both proper localization of T cells to “find” the melanocytes, and also increases their determination to kill them. There are existing drugs that have been developed by pharmaceutical companies that block the ability of CXCL10 to function in humans, and so they may be effective treatments in vitiligo. (See PDF of this article: Click Here)




    We have also begun to identify the signals produced by stressed melanocytes that activate immune cells. We believe that studying the communication between stressed melanocytes and immune cells will tell us how vitiligo gets started in the first place, and how to better prevent its onset and spread. Also part of this project is better understanding how chemicals in the environment cause stress in melanocytes. Certain chemicals are well known to cause vitiligo and make it worse, and it is likely that there are many more that we come into contact with every day (in chemical dyes, cleaning products, etc). While we can guess at which chemicals do this based on their chemical structure, we are using our systems to definitively identify the chemicals, so that patients can avoid them and companies can change the ingredients of their products.

     




     



    Collapse Rotation Projects

    Rotations:

    1. Targeting the IFN-?-chemokine axis for treatment of vitiligo: We are using our newly developed mouse model and human tissues from patients with vitiligo to identify the cytokines and chemokines that are expressed within the depigmenting skin and which skin cells produce them. We are using genetically modified mouse strains (knockouts, conditional knockouts, fluorescent reporter strains), and cytokine and chemokine neutralizing antibodies to identify the key proteins required for disease. This data will permit us to rationally develop and test new therapeutic agents.
    2. Understanding the proinflammatory signals generated by melanocytes under cellular stress. Melanocytes from vitiligo patients have intrinsic abnormalities, including cellular stress evidenced by increased production of reactive oxygen species (ROS) and activation of the unfolded protein response (UPR). The immune system has evolved to recognize this stress as damage-associated molecular patterns (DAMPs), which activate innate immunity. We are using human cells and tissues to determine how cellular stress, innate immunity, and adaptive immunity cooperate to initiate and perpetuate depigmentation in vitiligo.
    3. Developing a humanized mouse model of immune-skin interactions to serve as a pre-clinical bridge to clinical studies: We are developing a humanized mouse model of skin disease that consists of an immunodeficient mouse strain as a host for an autologous human skin graft and immune reconstitution in order to study mechanisms of inflammation in the skin, including allergic contact dermatitis, response to infection, tumor immunotherapy, and autoimmunity, all within a fully human environment. This model system will act as a pre-clinical bridge between mouse models and human clinical trials, providing an opportunity to test new treatments on human cells and tissues prior to initiating trials on patients.
    4. Tracking real-time autoreactive T cell migration and interactions within the skin: We are using fluorescently/bioluminescently tagged CD8 T cells to track their movements and interactions within the skin in live mice, using real-time confocal microscopy and bioluminescent imaging. Initial studies will focus on the role of cytokines and chemokines in T cell migration within the skin.
    5. Clinical trial to test a novel treatment for vitiligo: We are in the early stages of developing a clinical trial based on insights developed from our animal data to test a novel drug for its ability to treat vitiligo.



    Rotations:




    1. Targeting the IFN-g-chemokine axis for treatment of vitiligo: We are using our newly developed mouse model and human tissues from patients with vitiligo to identify the cytokines and chemokines that are expressed within the depigmenting skin and which skin cells produce them. We are using genetically modified mouse strains (knockouts, conditional knockouts, fluorescent reporter strains), and cytokine and chemokine neutralizing antibodies to identify the key proteins required for disease. This data will permit us to rationally develop and test new therapeutic agents.


    2. Understanding the proinflammatory signals generated by melanocytes under cellular stress. Melanocytes from vitiligo patients have intrinsic abnormalities, including cellular stress evidenced by increased production of reactive oxygen species (ROS) and activation of the unfolded protein response (UPR). The immune system has evolved to recognize this stress as damage-associated molecular patterns (DAMPs), which activate innate immunity. We are using human cells and tissues to determine how cellular stress, innate immunity, and adaptive immunity cooperate to initiate and perpetuate depigmentation in vitiligo.


    3. Developing a humanized mouse model of immune-skin interactions to serve as a pre-clinical bridge to clinical studies: We are developing a humanized mouse model of skin disease that consists of an immunodeficient mouse strain as a host for an autologous human skin graft and immune reconstitution in order to study mechanisms of inflammation in the skin, including allergic contact dermatitis, response to infection, tumor immunotherapy, and autoimmunity, all within a fully human environment. This model system will act as a pre-clinical bridge between mouse models and human clinical trials, providing an opportunity to test new treatments on human cells and tissues prior to initiating trials on patients.


    4. Tracking autoreactive T cell interactions within the skin: We are using fluorescently tagged CD8 T cells to track their cellular interactions within the skin using confocal microscopy. Future studies will adapt this model to investigate real-time migration and other movements of these cells within compartments of the skin.


    5. Clinical trial to test a novel treatment for vitiligo: We recently completed a clinical trial based on insights developed from our animal data to test a novel drug for its ability to treat vitiligo.






    Collapse Bibliographic 
    Collapse selected publications
    Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Faculty can login to make corrections and additions.
    List All   |   Timeline
    1. Riding RL, Harris JE. The Role of Memory CD8+ T Cells in Vitiligo. J Immunol. 2019 Jul 01; 203(1):11-19. PMID: 31209143.
      View in: PubMed
    2. Richmond JM, Strassner JP, Essien KI, Harris JE. T-cell positioning by chemokines in autoimmune skin diseases. Immunol Rev. 2019 May; 289(1):186-204. PMID: 30977191.
      View in: PubMed
    3. van Geel N, Wolkerstorfer A, Ezzedine K, Pandya AG, Bekkenk M, Grine L, Van Belle S, Lommerts JE, Hamzavi I, Harris JE, Eleftheriadou V, Esmat S, Kang HY, Kumarasinghe P, Lan CE, Parsad D, Raboobee N, Xiang LF, Suzuki T, Prinsen CA, Taieb A, Picardo M, Speeckaert R. Validation of a Physicians Global Assessment (PGA) tool for vitiligo extent: results of an international vitiligo expert meeting. Pigment Cell Melanoma Res. 2019 Apr 03. PMID: 30945409.
      View in: PubMed
    4. Tkachenko E, Refat MA, Balzano T, Maloney ME, Harris JE. Patient satisfaction and physician productivity in shared medical appointments for vitiligo. J Am Acad Dermatol. 2019 Mar 22. PMID: 30910662.
      View in: PubMed
    5. Frisoli ML, Harris JE. Treatment with Modified Heat Shock Protein Repigments Vitiligo Lesions in Sinclair Swine. J Invest Dermatol. 2018 Dec; 138(12):2505-2506. PMID: 30466536.
      View in: PubMed
    6. Richmond JM, Strassner JP, Rashighi M, Agarwal P, Garg M, Essien KI, Pell LS, Harris JE. Resident memory and recirculating memory T cells cooperate to maintain disease in a mouse model of vitiligo. J Invest Dermatol. 2018 Nov 10. PMID: 30423329.
      View in: PubMed
    7. Riding RL, Richmond JM, Harris JE. Mouse Model for Human Vitiligo. Curr Protoc Immunol. 2018 Sep 25; e63. PMID: 30253067.
      View in: PubMed
    8. Richmond JM, Strassner JP, Zapata L, Garg M, Riding RL, Refat MA, Fan X, Azzolino V, Tovar-Garza A, Tsurushita N, Pandya AG, Tso JY, Harris JE. Antibody blockade of IL-15 signaling has the potential to durably reverse vitiligo. Sci Transl Med. 2018 Jul 18; 10(450). PMID: 30021889.
      View in: PubMed
    9. Mande P, Zirak B, Ko WC, Taravati K, Bride KL, Brodeur TY, Deng A, Dresser K, Jiang Z, Ettinger R, Fitzgerald KA, Rosenblum MD, Harris JE, Marshak-Rothstein A. Fas ligand promotes an inducible TLR-dependent model of cutaneous lupus-like inflammation. J Clin Invest. 2018 Jun 11. PMID: 29889098.
      View in: PubMed
    10. Korta DZ, Christiano AM, Bergfeld W, Duvic M, Ellison A, Fu J, Harris JE, Hordinsky MK, King B, Kranz D, Mackay-Wiggan J, McMichael A, Norris DA, Price V, Shapiro J, Atanaskova Mesinkovska N. Alopecia areata is a medical disease. J Am Acad Dermatol. 2018 Apr; 78(4):832-834. PMID: 29548423.
      View in: PubMed
    11. Fukuda K, Harris JE. Vitiligo-like depigmentation in patients receiving programmed cell death-1 inhibitor reflects active vitiligo. J Am Acad Dermatol. 2018 01; 78(1):e15-e16. PMID: 29241799.
      View in: PubMed
    12. Kranz D, Ellison A, Mesinkovska NA, Christiano AM, Hordinsky MK, Harris JE. Building and Crossing the Translational Bridge: 2016 Alopecia Areata Research Summit Highlights. J Investig Dermatol Symp Proc. 2018 Jan; 19(1):S3-S8. PMID: 29273102.
      View in: PubMed
    13. Liu LY, Strassner JP, Refat MA, Harris JE, King BA. Repigmentation in vitiligo using the Janus kinase inhibitor tofacitinib may require concomitant light exposure. J Am Acad Dermatol. 2017 Oct; 77(4):675-682.e1. PMID: 28823882.
      View in: PubMed
    14. Frisoli ML, Harris JE. Vitiligo: Mechanistic insights lead to novel treatments. J Allergy Clin Immunol. 2017 Sep; 140(3):654-662. PMID: 28778794.
      View in: PubMed
    15. Rodrigues M, Ezzedine K, Hamzavi I, Pandya AG, Harris JE. Current and emerging treatments for vitiligo. J Am Acad Dermatol. 2017 Jul; 77(1):17-29. PMID: 28619557.
      View in: PubMed
    16. Rodrigues M, Ezzedine K, Hamzavi I, Pandya AG, Harris JE. New discoveries in the pathogenesis and classification of vitiligo. J Am Acad Dermatol. 2017 Jul; 77(1):1-13. PMID: 28619550.
      View in: PubMed
    17. Harris JE. Chemical-Induced Vitiligo. Dermatol Clin. 2017 Apr; 35(2):151-161. PMID: 28317525.
      View in: PubMed
    18. Rashighi M, Harris JE. Vitiligo Pathogenesis and Emerging Treatments. Dermatol Clin. 2017 Apr; 35(2):257-265. PMID: 28317534.
      View in: PubMed
    19. Harris JE. Optimizing Vitiligo Management: Past, Present, and Future. Dermatol Clin. 2017 Apr; 35(2):xi. PMID: 28317535.
      View in: PubMed
    20. Strassner JP, Rashighi M, Ahmed Refat M, Richmond JM, Harris JE. Suction blistering the lesional skin of vitiligo patients reveals useful biomarkers of disease activity. J Am Acad Dermatol. 2017 Mar 01. PMID: 28259440.
      View in: PubMed
    21. Mohammad TF, Al-Jamal M, Hamzavi IH, Harris JE, Leone G, Cabrera R, Lim HW, Pandya AG, Esmat SM. The Vitiligo Working Group recommendations for narrowband ultraviolet B light phototherapy treatment of vitiligo. J Am Acad Dermatol. 2017 Feb 15. PMID: 28216034.
      View in: PubMed
    22. Richmond JM, Masterjohn E, Chu R, Tedstone J, Youd ME, Harris JE. CXCR3 Depleting Antibodies Prevent and Reverse Vitiligo in Mice. J Invest Dermatol. 2017 Jan 23. PMID: 28126463.
      View in: PubMed
    23. Vanderweil SG, Amano S, Ko WC, Richmond JM, Kelley M, Senna MM, Pearson A, Chowdary S, Hartigan C, Barton B, Harris JE. A double-blind, placebo-controlled, phase-II clinical trial to evaluate oral simvastatin as a treatment for vitiligo. J Am Acad Dermatol. 2017 Jan; 76(1):150-151.e3. PMID: 27986135.
      View in: PubMed
    24. Rashighi M, Harris JE. Sampling Serum in Patients With Vitiligo to Measure Disease Activity in the Skin. JAMA Dermatol. 2016 Nov 1; 152(11):1187-1188. PMID: 27557448.
      View in: PubMed
    25. Strassner JP, Harris JE. Understanding mechanisms of autoimmunity through translational research in vitiligo. Curr Opin Immunol. 2016 Dec; 43:81-88. PMID: 27764715.
      View in: PubMed
    26. Chong SZ, Evrard M, Devi S, Chen J, Lim JY, See P, Zhang Y, Adrover JM, Lee B, Tan L, Li JL, Liong KH, Phua C, Balachander A, Boey A, Liebl D, Tan SM, Chan JK, Balabanian K, Harris JE, Bianchini M, Weber C, Duchene J, Lum J, Poidinger M, Chen Q, Rénia L, Wang CI, Larbi A, Randolph GJ, Weninger W, Looney MR, Krummel MF, Biswas SK, Ginhoux F, Hidalgo A, Bachelerie F, Ng LG. CXCR4 identifies transitional bone marrow premonocytes that replenish the mature monocyte pool for peripheral responses. J Exp Med. 2016 Oct 17; 213(11):2293-2314. PMID: 27811056.
      View in: PubMed
    27. Richmond JM, Bangari DS, Essien KI, Currimbhoy SD, Groom JR, Pandya AG, Youd ME, Luster AD, Harris JE. Keratinocyte-Derived Chemokines Orchestrate T-Cell Positioning in the Epidermis during Vitiligo and May Serve as Biomarkers of Disease. J Invest Dermatol. 2017 Feb; 137(2):350-358. PMID: 27686391.
      View in: PubMed
    28. Rork JF, Rashighi M, Harris JE. Understanding autoimmunity of vitiligo and alopecia areata. Curr Opin Pediatr. 2016 Aug; 28(4):463-9. PMID: 27191524.
      View in: PubMed
    29. Strassner JP, Rashighi M, Harris JE. Melanocytes in psoriasis: convicted culprit or bullied bystander? Pigment Cell Melanoma Res. 2016 May; 29(3):261-3. PMID: 26929278.
      View in: PubMed
    30. Li JL, Lim CH, Tay FW, Goh CC, Devi S, Malleret B, Lee B, Bakocevic N, Chong SZ, Evrard M, Tanizaki H, Lim HY, Russell B, Renia L, Zolezzi F, Poidinger M, Angeli V, St John AL, Harris JE, Tey HL, Tan SM, Kabashima K, Weninger W, Larbi A, Ng LG. Neutrophils Self-Regulate Immune Complex-Mediated Cutaneous Inflammation through CXCL2. J Invest Dermatol. 2016 Feb; 136(2):416-24. PMID: 26802238.
      View in: PubMed
    31. Harris JE. Cellular stress and innate inflammation in organ-specific autoimmunity: lessons learned from vitiligo. Immunol Rev. 2016 Jan; 269(1):11-25. PMID: 26683142.
      View in: PubMed
    32. Harris JE, Rashighi M, Nguyen N, Jabbari A, Ulerio G, Clynes R, Christiano AM, Mackay-Wiggan J. Rapid skin repigmentation on oral ruxolitinib in a patient with coexistent vitiligo and alopecia areata (AA). J Am Acad Dermatol. 2016 Feb; 74(2):370-1. PMID: 26685721.
      View in: PubMed
    33. Rashighi M, Harris JE. Interfering with the IFN-?/CXCL10 pathway to develop new targeted treatments for vitiligo. Ann Transl Med. 2015 Dec; 3(21):343. PMID: 26734651.
      View in: PubMed
    34. Harris JE. Melanocyte Regeneration in Vitiligo Requires WNT beneath their Wings. J Invest Dermatol. 2015 Dec; 135(12):2921-3. PMID: 26569586.
      View in: PubMed
    35. Ezzedine K, Sheth V, Rodrigues M, Eleftheriadou V, Harris JE, Hamzavi IH, Pandya AG. Vitiligo is not a cosmetic disease. J Am Acad Dermatol. 2015 Nov; 73(5):883-5. PMID: 26475548.
      View in: PubMed
    36. Zhang R, Borges CM, Fan MY, Harris JE, Turka LA. Requirement for CD28 in Effector Regulatory T Cell Differentiation, CCR6 Induction, and Skin Homing. J Immunol. 2015 Nov 01; 195(9):4154-61. PMID: 26408668.
      View in: PubMed
    37. Wu S, Li WQ, Cho E, Harris JE, Speizer F, Qureshi AA. Use of permanent hair dyes and risk of vitiligo in women. Pigment Cell Melanoma Res. 2015 Nov; 28(6):744-6. PMID: 26212072.
      View in: PubMed
    38. Harris JE. IFN-? in Vitiligo, Is It the Fuel or the Fire? Acta Derm Venereol. 2015 Jul; 95(6):643-4. PMID: 26059003.
      View in: PubMed
    39. Picardo M, Dell'Anna ML, Ezzedine K, Hamzavi I, Harris JE, Parsad D, Taieb A. Vitiligo. Nat Rev Dis Primers. 2015 06 04; 1:15011. PMID: 27189851.
      View in: PubMed
    40. Agarwal P, Rashighi M, Essien KI, Richmond JM, Randall L, Pazoki-Toroudi H, Hunter CA, Harris JE. Simvastatin prevents and reverses depigmentation in a mouse model of vitiligo. J Invest Dermatol. 2015 Apr; 135(4):1080-8. PMID: 25521459.
      View in: PubMed
    41. Richmond JM, Harris JE. Immunology and skin in health and disease. Cold Spring Harb Perspect Med. 2014 Dec 01; 4(12):a015339. PMID: 25452424.
      View in: PubMed
    42. Rashighi M, Agarwal P, Richmond JM, Harris TH, Dresser K, Su MW, Zhou Y, Deng A, Hunter CA, Luster AD, Harris JE. CXCL10 is critical for the progression and maintenance of depigmentation in a mouse model of vitiligo. Sci Transl Med. 2014 Feb 12; 6(223):223ra23. PMID: 24523323.
      View in: PubMed
    43. Harris JE. Vitiligo and alopecia areata: apples and oranges? Exp Dermatol. 2013 Dec; 22(12):785-9. PMID: 24131336.
      View in: PubMed
    44. Richmond JM, Frisoli ML, Harris JE. Innate immune mechanisms in vitiligo: danger from within. Curr Opin Immunol. 2013 Dec; 25(6):676-82. PMID: 24238922.
      View in: PubMed
    45. Malhotra N, Narayan K, Cho OH, Sylvia KE, Yin C, Melichar H, Rashighi M, Lefebvre V, Harris JE, Berg LJ, Kang J. A network of high-mobility group box transcription factors programs innate interleukin-17 production. Immunity. 2013 Apr 18; 38(4):681-93. PMID: 23562159.
      View in: PubMed
    46. Chin MS, Freniere BB, Fakhouri S, Harris JE, Lalikos JF, Crosby AJ. Cavitation rheology as a potential method for in vivo assessment of skin biomechanics. Plast Reconstr Surg. 2013 Feb; 131(2):303e-305e. PMID: 23358043.
      View in: PubMed
    47. Harris JE, Harris TH, Weninger W, Wherry EJ, Hunter CA, Turka LA. A mouse model of vitiligo with focused epidermal depigmentation requires IFN-? for autoreactive CD8? T-cell accumulation in the skin. J Invest Dermatol. 2012 Jul; 132(7):1869-76. PMID: 22297636.
      View in: PubMed
    48. Harris JE, Marshak-Rothstein A. Editorial: Interfering with B cell immunity. J Leukoc Biol. 2011 Jun; 89(6):805-6. PMID: 21628334.
      View in: PubMed
    49. Ramón HE, Cejas PJ, LaRosa D, Rahman A, Harris JE, Zhang J, Hunter C, Choi Y, Turka LA. EGR-2 is not required for in vivo CD4 T cell mediated immune responses. PLoS One. 2010 Sep 23; 5(9):e12904. PMID: 20886122.
      View in: PubMed
    50. Harris JE, Seykora JT, Lee RA. Renbok phenomenon and contact sensitization in a patient with alopecia universalis. Arch Dermatol. 2010 Apr; 146(4):422-5. PMID: 20404233.
      View in: PubMed
    51. Bishop KD, Harris JE, Mordes JP, Greiner DL, Rossini AA, Czech MP, Phillips NE. Depletion of the programmed death-1 receptor completely reverses established clonal anergy in CD4(+) T lymphocytes via an interleukin-2-dependent mechanism. Cell Immunol. 2009; 256(1-2):86-91. PMID: 19230866.
      View in: PubMed
    52. Harris JE, Sutton DA, Rubin A, Wickes B, De Hoog GS, Kovarik C. Exophiala spinifera as a cause of cutaneous phaeohyphomycosis: case study and review of the literature. Med Mycol. 2009 Feb; 47(1):87-93. PMID: 19101838.
      View in: PubMed
    53. Harris JE, Bishop KD, Phillips NE, Mordes JP, Greiner DL, Rossini AA, Czech MP. Early growth response gene-2, a zinc-finger transcription factor, is required for full induction of clonal anergy in CD4+ T cells. J Immunol. 2004 Dec 15; 173(12):7331-8. PMID: 15585857.
      View in: PubMed
    54. Hemavathy K, Guru SC, Harris J, Chen JD, Ip YT. Human Slug is a repressor that localizes to sites of active transcription. Mol Cell Biol. 2000 Jul; 20(14):5087-95. PMID: 10866665.
      View in: PubMed
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