Rikard Holmdahl
Karolinska Institutet
674 Papers
7.3K Citations
Rikard Holmdahl is an academic researcher from Karolinska Institutet. The author has contributed to research in topics: Arthritis & T cell. The author has an hindex of 91, co-authored 644 publications. Previous affiliations of Rikard Holmdahl include Umeå University & University of Erlangen-Nuremberg.
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Papers
Perforin deficiency attenuates collagen-induced arthritis
Kristin Bauer,Annika Knipper,Hoang Tu-Rapp,Dirk Koczan,Hans-Jürgen Kreutzer,Horst Nizze,Eilhard Mix,Hans-Juergen Thiesen,Rikard Holmdahl,Saleh M. Ibrahim +9 more
TL;DR: Pfp-mediated cytotoxicity is involved in the initiation of tissue damage in arthritis, but pfp-independent cytotoxic death pathways might also contribute to CIA.
Antigen-specific gene therapy after immunisation reduces the severity of collagen-induced arthritis
Tove Eneljung,Sara Tengvall,Pernilla Jirholt,Louise Henningsson,Rikard Holmdahl,Kenth Gustafsson,Inger Gjertsson +6 more
TL;DR: A model of antigen-specific tolerance in collagen type II (CII) induced arthritis (CIA) using lentivirus-based gene therapy is developed and offers a good model for investigation of the basic mechanisms during tolerance in CIA.
Chemical changes demonstrated in cartilage by synchrotron infrared microspectroscopy in an antibody-induced murine model of rheumatoid arthritis
Allyson M. Croxford,Kutty Selva Nandakumar,Rikard Holmdahl,Mark J. Tobin,Donald McNaughton,Merrill J. Rowley +5 more
TL;DR: The utility of synchrotron FTIRM is demonstrated for examining chemical changes in diseased cartilage at the microscopic level and it is established that arthritogenic mAbs to CII do cause cartilage damage in vivo in the absence of inflammation.
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Characterization of the anticollagen antibody response in a new model of chronic polyarthritis.
Paola Conigliaro,Robert A. Benson,Agapitos Patakas,Sharon M. Kelly,Guido Valesini,Rikard Holmdahl,James M. Brewer,Iain B. McInnes,Paul Garside +8 more
TL;DR: The findings indicate that the development and severity of chronic disease is dependent on the antigen and is associated with an increased autoreactive B cell response directed against a specific CII epitope (U1).
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