James G. Krueger mainly investigates Immunology, Psoriasis, Immune system, Interleukin 17 and Tumor necrosis factor alpha. Immunology is closely attributed to Disease in his work. James G. Krueger interconnects Surgery, Internal medicine, Risankizumab and Keratinocyte in the investigation of issues within Psoriasis.
His work in Keratinocyte addresses subjects such as Dermis, which are connected to disciplines such as Molecular biology. His Immune system research includes themes of Myeloid and Genetic predisposition. His Interleukin 17 research is multidisciplinary, relying on both Interleukin, Interleukin 22, Keratin 16 and Interferon gamma.
Immunology, Psoriasis, Atopic dermatitis, Immune system and Pathology are his primary areas of study. Immunology is frequently linked to Disease in his study. James G. Krueger has researched Psoriasis in several fields, including Tumor necrosis factor alpha, Internal medicine and Interleukin 17.
His work carried out in the field of Internal medicine brings together such families of science as Gastroenterology, Endocrinology and Oncology. His research on Immune system focuses in particular on Dendritic cell. His Pathology study often links to related topics such as Keratinocyte.
James G. Krueger mostly deals with Psoriasis, Immunology, Atopic dermatitis, Internal medicine and Dermatology. His study focuses on the intersection of Psoriasis and fields such as Interferon with connections in the field of Tyrosine kinase 2. His Immune system, Cytokine, Dendritic cell, Chemokine and Filaggrin study are his primary interests in Immunology.
His Atopic dermatitis research incorporates elements of Biomarker, T cell, Systemic inflammation and SCORAD. His studies in Internal medicine integrate themes in fields like Gastroenterology and Oncology. In his study, Adalimumab and Brodalumab is inextricably linked to Hidradenitis suppurativa, which falls within the broad field of Dermatology.
His primary areas of study are Immunology, Atopic dermatitis, Psoriasis, Internal medicine and Inflammation. His works in Cytokine, Immune system, Dendritic cell, Interleukin and Filaggrin are all subjects of inquiry into Immunology. James G. Krueger has included themes like Immunohistochemistry, SCORAD, Disease, Biomarker and Immunoglobulin E in his Atopic dermatitis study.
James G. Krueger studies Psoriasis Area and Severity Index which is a part of Psoriasis. His Internal medicine research focuses on subjects like Gastroenterology, which are linked to Area under the curve and Keratin 16. The study incorporates disciplines such as Skin biopsy, Endothelium and Pathogenesis in addition to Inflammation.
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Pathogenesis and therapy of psoriasis
Michelle A. Lowes;Anne M. Bowcock;James G. Krueger.
Nature (2007)
Psoriasis vulgaris lesions contain discrete populations of Th1 and Th17 T cells.
Michelle A. Lowes;Toyoko Kikuchi;Judilyn Fuentes-Duculan;Irma Cardinale.
Journal of Investigative Dermatology (2008)
Immunology of Psoriasis
Michelle A Lowes;Mayte Suárez-Fariñas;James G Krueger.
Annual Review of Immunology (2014)
Brodalumab, an Anti–Interleukin-17–Receptor Antibody for Psoriasis
Kim A Papp;Craig Leonardi;Alan Menter;Jean-Paul Ortonne.
The New England Journal of Medicine (2012)
Increased Expression of Interleukin 23 p19 and p40 in Lesional Skin of Patients with Psoriasis Vulgaris
Edmund Jd Lee;William L. Trepicchio;Judith L Oestreicher;Debra D Pittman.
Journal of Experimental Medicine (2004)
Interleukin 6 is expressed in high levels in psoriatic skin and stimulates proliferation of cultured human keratinocytes.
Rachel M. Grossman;James Krueger;Debra Yourish;Angela Granelli-Piperno.
Proceedings of the National Academy of Sciences of the United States of America (1989)
The immunologic basis for the treatment of psoriasis with new biologic agents
James G. Krueger.
Journal of The American Academy of Dermatology (2002)
Th17 cytokines interleukin (IL)-17 and IL-22 modulate distinct inflammatory and keratinocyte-response pathways.
K.E. Nograles;L.C. Zaba;E. Guttman-Yassky;J. Fuentes-Duculan.
British Journal of Dermatology (2008)
CTLA4Ig-mediated blockade of T cell costimulation in patients with psoriasis vulgaris
Judith R. Abrams;Mark G. Lebwohl;Cynthia A. Guzzo;Brian V. Jegasothy.
Journal of Clinical Investigation (1999)
Psoriasis pathophysiology: current concepts of pathogenesis
J G Krueger;A Bowcock.
Annals of the Rheumatic Diseases (2005)
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