James Krueger

Summary

Affiliation: The Rockefeller University
Country: USA

Publications

  1. pmc Alefacept (anti-CD2) causes a selective reduction in circulating effector memory T cells (Tem) and relative preservation of central memory T cells (Tcm) in psoriasis
    Francesca Chamian
    Laboratory for Investigative Dermatology, The Rockefeller University, New York, USA
    J Transl Med 5:27. 2007
  2. pmc Psoriasis vulgaris flare during efalizumab therapy does not preclude future use: a case series
    Michelle A Lowes
    Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY, USA
    BMC Dermatol 5:9. 2005
  3. pmc Eruptive papules during efalizumab (anti-CD11a) therapy of psoriasis vulgaris: a case series
    Michelle A Lowes
    Laboratory for Investigative Dermatology, The Rockefeller University, New York, New York, USA
    BMC Dermatol 7:2. 2007
  4. pmc Psoriasis pathophysiology: current concepts of pathogenesis
    J G Krueger
    Laboratory for Investigative Dermatology, Rockefeller University, 1230 York Ave, New York, NY 10021, USA
    Ann Rheum Dis 64:ii30-6. 2005
  5. doi request reprint Effect of therapeutic integrin (CD11a) blockade with efalizumab on immune responses to model antigens in humans: results of a randomized, single blind study
    James G Krueger
    Laboratory for Investigative Dermatology, Rockefeller University, New York, New York 10065, USA
    J Invest Dermatol 128:2615-24. 2008
  6. ncbi request reprint Psoriasis: evolution of pathogenic concepts and new therapies through phases of translational research
    E Guttman-Yassky
    Laboratory for Investigative Dermatology, The Rockefeller University, Box 178, 1230 York Avenue, New York, NY 10021, USA Guttman Yassky
    Br J Dermatol 157:1103-15. 2007
  7. ncbi request reprint Successful in vivo blockade of CD25 (high-affinity interleukin 2 receptor) on T cells by administration of humanized anti-Tac antibody to patients with psoriasis
    J G Krueger
    Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY 10021 6399, USA
    J Am Acad Dermatol 43:448-58. 2000
  8. ncbi request reprint The majority of epidermal T cells in Psoriasis vulgaris lesions can produce type 1 cytokines, interferon-gamma, interleukin-2, and tumor necrosis factor-alpha, defining TC1 (cytotoxic T lymphocyte) and TH1 effector populations: a type 1 differentiation bi
    L M Austin
    Laboratory of Investigative Dermatology, The Rockerfeller University, New York, New York 10021 6399, USA
    J Invest Dermatol 113:752-9. 1999
  9. pmc Th17 cytokines interleukin (IL)-17 and IL-22 modulate distinct inflammatory and keratinocyte-response pathways
    K E Nograles
    Laboratory of Investigative Dermatology, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA
    Br J Dermatol 159:1092-102. 2008
  10. ncbi request reprint Trimethylpsoralen bath PUVA is a remittive treatment for psoriasis vulgaris. Evidence that epidermal immunocytes are direct therapeutic targets
    T R Coven
    Laboratory for Investigative Dermatology, Rockefeller University, New York, NY, USA
    Arch Dermatol 134:1263-8. 1998

Research Grants

Collaborators

Detail Information

Publications50

  1. pmc Alefacept (anti-CD2) causes a selective reduction in circulating effector memory T cells (Tem) and relative preservation of central memory T cells (Tcm) in psoriasis
    Francesca Chamian
    Laboratory for Investigative Dermatology, The Rockefeller University, New York, USA
    J Transl Med 5:27. 2007
    ..Alefacept (anti-CD2) biological therapy selectively targets effector memory T cells (Tem) in psoriasis vulgaris, a model Type 1 autoimmune disease...
  2. pmc Psoriasis vulgaris flare during efalizumab therapy does not preclude future use: a case series
    Michelle A Lowes
    Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY, USA
    BMC Dermatol 5:9. 2005
    ..Severe psoriasis vulgaris can be extremely difficult to treat in some patients, even with the newer biological therapies available today...
  3. pmc Eruptive papules during efalizumab (anti-CD11a) therapy of psoriasis vulgaris: a case series
    Michelle A Lowes
    Laboratory for Investigative Dermatology, The Rockefeller University, New York, New York, USA
    BMC Dermatol 7:2. 2007
    ..Newer biological therapies for moderate-to-severe psoriasis are being used more frequently, but unexpected effects may occur...
  4. pmc Psoriasis pathophysiology: current concepts of pathogenesis
    J G Krueger
    Laboratory for Investigative Dermatology, Rockefeller University, 1230 York Ave, New York, NY 10021, USA
    Ann Rheum Dis 64:ii30-6. 2005
    ..This short review presents current pathogenic concepts that have emerged from genetic, genomic, and cellular information obtained in basic studies and from clinical studies of selective immune targeting drugs...
  5. doi request reprint Effect of therapeutic integrin (CD11a) blockade with efalizumab on immune responses to model antigens in humans: results of a randomized, single blind study
    James G Krueger
    Laboratory for Investigative Dermatology, Rockefeller University, New York, New York 10065, USA
    J Invest Dermatol 128:2615-24. 2008
    ..These results expand our knowledge of how immune responses are modulated in humans by CD11a blockade and have implications for vaccinations of patients treated with this agent...
  6. ncbi request reprint Psoriasis: evolution of pathogenic concepts and new therapies through phases of translational research
    E Guttman-Yassky
    Laboratory for Investigative Dermatology, The Rockefeller University, Box 178, 1230 York Avenue, New York, NY 10021, USA Guttman Yassky
    Br J Dermatol 157:1103-15. 2007
    ....
  7. ncbi request reprint Successful in vivo blockade of CD25 (high-affinity interleukin 2 receptor) on T cells by administration of humanized anti-Tac antibody to patients with psoriasis
    J G Krueger
    Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY 10021 6399, USA
    J Am Acad Dermatol 43:448-58. 2000
    ..Because IL-2 is a major stimulus for T-cell growth, blockade of the IL-2 receptor could be useful in treating T-cell-mediated (autoimmune) diseases...
  8. ncbi request reprint The majority of epidermal T cells in Psoriasis vulgaris lesions can produce type 1 cytokines, interferon-gamma, interleukin-2, and tumor necrosis factor-alpha, defining TC1 (cytotoxic T lymphocyte) and TH1 effector populations: a type 1 differentiation bi
    L M Austin
    Laboratory of Investigative Dermatology, The Rockerfeller University, New York, New York 10021 6399, USA
    J Invest Dermatol 113:752-9. 1999
    ....
  9. pmc Th17 cytokines interleukin (IL)-17 and IL-22 modulate distinct inflammatory and keratinocyte-response pathways
    K E Nograles
    Laboratory of Investigative Dermatology, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA
    Br J Dermatol 159:1092-102. 2008
    ..Psoriasis vulgaris is an inflammatory skin disease mediated by Th1 and Th17 cytokines, yet the relative contribution of interferon (IFN)-gamma, interleukin (IL)-17 and IL-22 on disease pathogenesis is still unknown...
  10. ncbi request reprint Trimethylpsoralen bath PUVA is a remittive treatment for psoriasis vulgaris. Evidence that epidermal immunocytes are direct therapeutic targets
    T R Coven
    Laboratory for Investigative Dermatology, Rockefeller University, New York, NY, USA
    Arch Dermatol 134:1263-8. 1998
    ....
  11. ncbi request reprint PUVA-induced lymphocyte apoptosis: mechanism of action in psoriasis
    T R Coven
    Laboratory of Investigative Dermatology, Rockefeller University, New York, NY 10021 6399, USA
    Photodermatol Photoimmunol Photomed 15:22-7. 1999
    ..If further investigation supports TMP's lack of carcinogenicity, this potent lymphotoxic treatment may prove to be one of the safest and most effective treatments for psoriasis...
  12. ncbi request reprint Role of the immune system and immunological circuits in psoriasis
    A Jabbari
    The Ronald O Perelman, Department of Dermatology, New York University School of MedicineNew York, NY, USA
    G Ital Dermatol Venereol 146:17-30. 2011
    ..Furthermore, these recent advances have been fruitful in leading to the development of new classes of biologic therapeutics that are remarkably effective in halting the disease process...
  13. ncbi request reprint An open-label, single-arm pilot study in patients with severe plaque-type psoriasis treated with an oral anti-inflammatory agent, apremilast
    A B Gottlieb
    Department of Dermatology, Tufts University, Boston, MA 02111 1533, USA
    Curr Med Res Opin 24:1529-38. 2008
    ..To evaluate the clinical and biological activity of apremilast in patients with severe plaque-type psoriasis...
  14. ncbi request reprint Major differences in inflammatory dendritic cells and their products distinguish atopic dermatitis from psoriasis
    Emma Guttman-Yassky
    Laboratory for Investigative Dermatology, Rockefeller University, New York, NY 10021, USA
    J Allergy Clin Immunol 119:1210-7. 2007
    ..Both diseases have been associated with increased numbers of dendritic cells (DCs) in the skin, but the similarities and differences in DC populations need to be established...
  15. ncbi request reprint Effects of etanercept are distinct from infliximab in modulating proinflammatory genes in activated human leukocytes
    Asifa S Haider
    Laboratory of Investigative Dermatology, Rockefeller University, New York, New York 10021, USA
    J Investig Dermatol Symp Proc 12:9-15. 2007
    ....
  16. ncbi request reprint Characterization of the divergent wound-healing responses occurring in the pathergy reaction and normal healthy volunteers
    Melike Melikoglu
    Cerrahpasa Medical Faculty, University of Istanbul, Istanbul, Turkey
    J Immunol 177:6415-21. 2006
    ....
  17. ncbi request reprint Novel insight into the agonistic mechanism of alefacept in vivo: differentially expressed genes may serve as biomarkers of response in psoriasis patients
    Asifa S Haider
    Laboratory for Investigative Dermatology, Rockefeller University, New York, NY 10021, USA
    J Immunol 178:7442-9. 2007
    ....
  18. ncbi request reprint Pathogenesis and therapy of psoriasis
    Michelle A Lowes
    Laboratory for Investigative Dermatology, The Rockefeller University, 1230 York Avenue, Box 178, New York, New York 10021, USA
    Nature 445:866-73. 2007
    ..The newest therapies for psoriasis target its immune components and may predict potential treatments for other inflammatory human diseases...
  19. pmc Normal human dermis contains distinct populations of CD11c+BDCA-1+ dendritic cells and CD163+FXIIIA+ macrophages
    Lisa C Zaba
    Laboratory for Investigative Dermatology, The Rockefeller University, New York, New York 10021, USA
    J Clin Invest 117:2517-25. 2007
    ..In summary, the normal dermis contains typical immunostimulatory myeloid DCs identified by CD11c and BDCA-1, as well as an additional population of poorly stimulatory macrophages marked by CD163 and FXIIIA...
  20. ncbi request reprint Cellular genomic maps help dissect pathology in human skin disease
    Asifa S Haider
    Laboratory of Investigative Dermatology, The Rockefeller University, New York, New York 10021 6399, USA
    J Invest Dermatol 128:606-15. 2008
    ..We were able to ascribe over 90% of these genes to specific cell types, and there was a surprisingly large contribution from DCs. This shows the utility of such cellular gene maps...
  21. ncbi request reprint Insights into gene modulation by therapeutic TNF and IFNgamma antibodies: TNF regulates IFNgamma production by T cells and TNF-regulated genes linked to psoriasis transcriptome
    Asifa S Haider
    Department of Investigative Dermatology, Laboratory of Investigative Dermatology, The Rockefeller University, New York, New York 10021, USA
    J Invest Dermatol 128:655-66. 2008
    ..These data suggest that TNF blockade with infliximab can suppress a major pathway of the adaptive immune response and this observation provides a key rationale for targeting TNF in "Type-1" T-cell-mediated autoimmune diseases...
  22. pmc Amelioration of epidermal hyperplasia by TNF inhibition is associated with reduced Th17 responses
    Lisa C Zaba
    Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY 10065, USA
    J Exp Med 204:3183-94. 2007
    ..Th17 cells may be particularly important in driving epidermal activation in psoriatic plaques, whereas Th1 cells must also be eliminated for final disease resolution...
  23. doi request reprint Psoriasis vulgaris lesions contain discrete populations of Th1 and Th17 T cells
    Michelle A Lowes
    Laboratory for Investigative Dermatology, The Rockefeller University, New York, New York 10021, USA
    J Invest Dermatol 128:1207-11. 2008
    ..Our findings suggest that psoriasis is a mixed Th1 and Th17 inflammatory environment. Th17 cells may be proximal regulators of psoriatic skin inflammation, and warrant further attention as therapeutic targets...
  24. ncbi request reprint Psoriasis as a model for T-cell-mediated disease: immunobiologic and clinical effects of treatment with multiple doses of efalizumab, an anti-CD11a antibody
    Alice B Gottlieb
    University of Medicine and Dentistry of New Jersey Robert Wood Johnson Medical School, Clinical Research Center, New Brunswick, NJ 08903 0019, USA
    Arch Dermatol 138:591-600. 2002
    ..Leukocyte function-associated antigen 1 (LFA-1), consisting of CD11a and CD18 subunits, plays an important role in T-cell activation and leukocyte extravasation...
  25. doi request reprint Blockade of CD11a by efalizumab in psoriasis patients induces a unique state of T-cell hyporesponsiveness
    Emma Guttman-Yassky
    Laboratory for Investigative Dermatology, The Rockefeller University, New York, New York 10065, USA
    J Invest Dermatol 128:1182-91. 2008
    ..The nature of this T-cell hyporesponsiveness suggests that T-cell responses may be reduced during efalizumab therapy, but are reversible after ceasing efalizumab treatment...
  26. ncbi request reprint Identification of cellular pathways of "type 1," Th17 T cells, and TNF- and inducible nitric oxide synthase-producing dendritic cells in autoimmune inflammation through pharmacogenomic study of cyclosporine A in psoriasis
    Asifa S Haider
    Laboratory for Investigative Dermatology, Rockefeller University, New York, NY, 10021, USA
    J Immunol 180:1913-20. 2008
    ..In addition, these data also identify new gene targets for therapeutic modulation and may be applied to wide range of autoimmune diseases...
  27. ncbi request reprint Etanercept induces apoptosis of dermal dendritic cells in psoriatic plaques of responding patients
    Rama Malaviya
    Division of Clinical Pharmacology, University of Medicine and Dentistry of New Jersey Robert Wood Johnson Medical School, New Brunswick 08903 0019, USA
    J Am Acad Dermatol 55:590-7. 2006
    ..We hypothesized that etanercept decreases inflammatory cell infiltration by inducing apoptosis...
  28. ncbi request reprint Prominent production of IL-20 by CD68+/CD11c+ myeloid-derived cells in psoriasis: Gene regulation and cellular effects
    Frank Wang
    Laboratory for Investigative Dermatology, The Rockefeller University, New York, New York 10021, USA
    J Invest Dermatol 126:1590-9. 2006
    ..Hence, IL-20 may influence inflammation through IFN-like effects. Together, these data indicate that IL-20 may be an important effector cytokine in psoriasis, and that its inhibition may represent a potential therapeutic target...
  29. ncbi request reprint The immunologic basis for the treatment of psoriasis with new biologic agents
    James G Krueger
    Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY 10021 6399, USA
    J Am Acad Dermatol 46:1-23; quiz 23-6. 2002
    ..In turn, each of these steps offers an opportunity for intervention with engineered biologic therapeutics...
  30. ncbi request reprint A putative RUNX1 binding site variant between SLC9A3R1 and NAT9 is associated with susceptibility to psoriasis
    Cynthia Helms
    Department of Genetics, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Nat Genet 35:349-56. 2003
    ..This is the second example of loss of a RUNX1 binding site associated with susceptibility to an autoimmune disease. It also suggests defective regulation of SLC9A3R1 or NAT9 by RUNX1 as a susceptibility factor for psoriasis...
  31. pmc Increased expression of interleukin 23 p19 and p40 in lesional skin of patients with psoriasis vulgaris
    Edmund Lee
    Laboratory for Investigative Dermatology, The Rockefeller University Hospital, P O Box 178, 1230 York Avenue, New York, NY 10021, USA
    J Exp Med 199:125-30. 2004
    ..Our data suggest that IL-23 is playing a more dominant role than IL-12 in psoriasis, a Th1 type of human inflammatory disease...
  32. ncbi request reprint Combining several ordinal measures in clinical studies
    Knut M Wittkowski
    General Clinical Research Center, The Rockefeller University, New York, NY 10021, USA
    Stat Med 23:1579-92. 2004
    ..The scoring method is demonstrated to be applicable to scoring clinical response profiles in the treatment of psoriasis and then to identifying genomic pathways that best correlate with these profiles...
  33. ncbi request reprint Psoriasis vulgaris: cutaneous lymphoid tissue supports T-cell activation and "Type 1" inflammatory gene expression
    Wook Lew
    Department of Dermatology, Yonsei University College of Medicine, Yongdong Severance Hospital, 146 29 Dogok Dong, Kangman Ku, Seoul, South Korea
    Trends Immunol 25:295-305. 2004
  34. ncbi request reprint Narrowband (312-nm) UV-B suppresses interferon gamma and interleukin (IL) 12 and increases IL-4 transcripts: differential regulation of cytokines at the single-cell level
    Ian B Walters
    Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY 10021 6399, USA
    Arch Dermatol 139:155-61. 2003
    ..To determine whether 312-nm UV-B alters production of effector and regulatory cytokines by viable T cells that remain in psoriatic lesions during UV-B phototherapy...
  35. ncbi request reprint Psoriasis vulgaris: an interplay of T lymphocytes, dendritic cells, and inflammatory cytokines in pathogenesis
    Francesca Chamian
    Laboratory for Investigative Dermatology, Rockefeller University, New York, New York 10021, USA
    Curr Opin Rheumatol 16:331-7. 2004
    ..Discuss and update concepts and hypotheses for the pathogenesis of psoriasis based on new research reports (primarily from 2003 and early 2004)...
  36. ncbi request reprint Efalizumab (anti-CD11a)-induced increase in peripheral blood leukocytes in psoriasis patients is preferentially mediated by altered trafficking of memory CD8+ T cells into lesional skin
    Yulia Vugmeyster
    Genentech, Inc, South San Francisco, CA, USA
    Clin Immunol 113:38-46. 2004
    ..The relatively smaller increase in naive peripheral blood T cells could be attributed to reduced trafficking of naive T cells...
  37. ncbi request reprint Current concepts in the immunopathogenesis of psoriasis
    Michelle A Lowes
    Rockefeller University, 1230 York Avenue, Box 178, New York, NY 10021, USA
    Dermatol Clin 22:349-69, vii. 2004
    ..Finally, pathogenic contributions from important psoriatic mouse models and recent genomic data using the new gene chip technology are elaborated...
  38. pmc Alefacept reduces infiltrating T cells, activated dendritic cells, and inflammatory genes in psoriasis vulgaris
    Francesca Chamian
    Laboratory for Investigative Dermatology, The Rockefeller University, 1230 York Avenue, New York, NY 10021
    Proc Natl Acad Sci U S A 102:2075-80. 2005
    ..Because we observed that alefacept binds primarily to T cells and not DCs, we suggest that T cells are the primary target for therapy, but that DCs and a spectrum of type 1 inflammatory genes are coordinately suppressed...
  39. ncbi request reprint Treatment of inflammatory dermatoses with novel biologic agents: a primer
    Rachel Nussbaum
    Laboratory for Investigative Dermatology, Rockefeller University, New York, NY, USA
    Adv Dermatol 18:45-89. 2002
  40. ncbi request reprint TNF inhibition rapidly down-regulates multiple proinflammatory pathways in psoriasis plaques
    Alice B Gottlieb
    Clinical Research Center, University of Medicine and Dentistry of New Jersey Robert Wood Johnson Medical School, New Brunswick, NJ 08901, USA
    J Immunol 175:2721-9. 2005
    ..This results in reversal of the epidermal hyperplasia and cutaneous inflammation characteristic of psoriatic plaques...
  41. ncbi request reprint Thalidomide induces granuloma differentiation in sarcoid skin lesions associated with disease improvement
    Stephen J Oliver
    The Laboratory of Cellular Physiology and Immunology, The Rockefeller University, New York, New York 10021, USA
    Clin Immunol 102:225-36. 2002
    ..Our data suggest that thalidomide treatment of sarcoidosis results in granuloma differentiation to a Th1-type cellular immune response usually associated with protective immunity to tuberculosis and tuberculoid leprosy...
  42. pmc Increase in TNF-alpha and inducible nitric oxide synthase-expressing dendritic cells in psoriasis and reduction with efalizumab (anti-CD11a)
    Michelle A Lowes
    Laboratory for Investigative Dermatology and Laboratory of Cellular Physiology and Immunology, The Rockefeller University, New York, NY 10021, USA
    Proc Natl Acad Sci U S A 102:19057-62. 2005
    ....
  43. ncbi request reprint Pharmacokinetics and pharmacodynamics of multiple weekly subcutaneous efalizumab doses in patients with plaque psoriasis
    Deborah L Mortensen
    Genentech, Inc, 1 DNA Way, South San Francisco, CA 94080 4990, USA
    J Clin Pharmacol 45:286-98. 2005
    ..Maximal pharmacodynamic effects were sustained at both dose levels through the course of treatment and were commensurate with improvements in psoriasis...
  44. ncbi request reprint Novel mechanisms of T-cell and dendritic cell activation revealed by profiling of psoriasis on the 63,100-element oligonucleotide array
    Xianghong Zhou
    Department of Biostatistics, Harvard University, Boston 02115, USA
    Physiol Genomics 13:69-78. 2003
    ....
  45. pmc Analytical approaches to reporting long-term clinical trial data
    Kim A Papp
    Probity Medical Research, Waterloo, ON, Canada
    Curr Med Res Opin 24:2001-8. 2008
    ..Therefore, standard analytical strategies used in short-term randomized, controlled trials (intent-to-treat, per-protocol) may not always be appropriate for data generated in long-term studies...
  46. ncbi request reprint A 50% reduction in the Psoriasis Area and Severity Index (PASI 50) is a clinically significant endpoint in the assessment of psoriasis
    Christopher S Carlin
    Department of Dermatology, University of Utah Health Sciences Center, Salt Lake City, Utah 84132, USA
    J Am Acad Dermatol 50:859-66. 2004
    ..We conclude that PASI 50 equates to a clinically meaningful improvement in psoriasis and represents a discerning primary endpoint...
  47. ncbi request reprint Human basal cell carcinoma is associated with Foxp3+ T cells in a Th2 dominant microenvironment
    Helen G Kaporis
    Laboratory for Investigative Dermatology, Rockefeller University, New York, New York, USA
    J Invest Dermatol 127:2391-8. 2007
    ..A better understanding of these opposing forces within the immune microenvironment may facilitate development of more potent immune-based treatment for BCC and other human carcinomas...
  48. ncbi request reprint Getting under the skin: the immunogenetics of psoriasis
    Anne M Bowcock
    Department of Genetics, Washington University School of Medicine, Saint Louis, Missouri 63110, USA
    Nat Rev Immunol 5:699-711. 2005
    ....
  49. ncbi request reprint Increased JunB mRNA and protein expression in psoriasis vulgaris lesions
    Asifa S Haider
    J Invest Dermatol 126:912-4. 2006
  50. ncbi request reprint Genomic analysis defines a cancer-specific gene expression signature for human squamous cell carcinoma and distinguishes malignant hyperproliferation from benign hyperplasia
    Asifa S Haider
    Laboratory of Investigative Dermatology, Rockefeller University, New York, New York, USA
    J Invest Dermatol 126:869-81. 2006
    ..The current study defines a unique gene expression signature for cutaneous SCC in humans and suggests potential roles for WNT, FZD, and PTN in the pathogenesis of SCC...

Research Grants8

  1. Therapeutic immune mechanisms of anti-CD11a in psoriasis
    James Krueger; Fiscal Year: 2004
    ..Following anti-CD1la we will look for reductions in 1) disease-associated T-cell activation, 2) Type 1 T-cells, and 3) abundance of specific, antigen-reactive T-cells in the peripheral circulation. ..
  2. Therapeutic immune mechanisms of daclizumab in psoriasis
    James Krueger; Fiscal Year: 2004
    ..We will also measure the impact of daclizumab on T cell activation/deviation towards Type 2 T cells by sensitive flow cytometry based assays. ..