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16 results on '"Holmdahl, Meirav"'

6. Additional file of Cystatin C influences the autoimmune but not inflammatory response to cartilage type II collagen leading to chronic arthritis development

Author

Bäcklund, Alexandra, Holmdahl, Meirav, Mattsson, Ragnar, Håkansson, Katarina, Lindström, Veronica, Kutty Selva Nandakumar, Grubb, Anders, and Holmdahl, Rikard

Subjects
urologic and male genital diseases, reproductive and urinary physiology, female genital diseases and pregnancy complications
Abstract

Additional file of Cystatin C influences the autoimmune but not inflammatory response to cartilage type II collagen leading to chronic arthritis development

Published
2021
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11. Primed B cells present type-II collagen to T cells

Author

Holmdahl, Meirav, Vestberg, Mikael, and Holmdahl, Rikard

Subjects
musculoskeletal diseases, T-Lymphocytes, physiology [B-Lymphocytes], Antigen-Presenting Cells, chemical and pharmacologic phenomena, macromolecular substances, Inbred C57BL, Antibodies, immunology [T-Lymphocytes], immunology [Collagen Type II], Mice, immunology [Antibodies], Animals, Inbred DBA, Non-U.S. Gov't, Collagen Type II, B-Lymphocytes, Animal, Arthritis, Macrophages, Immunology in the medical area, physiology [Macrophages], physiology [Antigen-Presenting Cells], Mice, Inbred C57BL, Mice, Inbred DBA, Support, etiology [Arthritis]
Abstract

Development of type-II collagen (CII)-induced arthritis (CIA) is dependent on a T-cell mediated activation of autoreactive B cells. However, it is still unclear if B cells can present CII to T cells. To investigate the role of B cells as antigen-presenting cells (APCs) for CII, we purified B cells from lymph nodes of immunized and nonimmunized mice. These B cells were used as APC for antigen-specific T-cell hybridomas. B cells from naïve mice did present native, triple-helical, CII (nCII) but also ovalbumin (OVA) and denatured CII (dCII) to antigen-specific T-cell hybridomas. In addition, B cells primed with nCII or OVA, but not dCII, activated the antigen-specific T-cell hybridomas two to three times better than naïve B cells. We conclude that antigen-primed B cells have the capacity to process and present CII to primed T cells, and antigen-primed antigen-specific B cells are more efficient as APC than naïve B cells. We further conclude that B cells have the potential to play an important role as APC in the development of CIA.

Published
2002

12. The major T cell epitope on type II collagen is glycosylated in normal cartilage but modified by arthritis in both rats and humans

Author

Dzhambazov, Balik, Holmdahl, Meirav, Yamada, Hisakata, Lu, Shemin, Vestberg, Mikael, Holm, Björn, Johnell, Olof, Kihlberg, Jan, Dzhambazov, Balik, Holmdahl, Meirav, Yamada, Hisakata, Lu, Shemin, Vestberg, Mikael, Holm, Björn, Johnell, Olof, and Kihlberg, Jan

Abstract

Type II collagen (CII) is a target for autoreactive T cells in both rheumatoid arthritis and the murine model collagen-induced arthritis. The determinant core of CII has been identified as CII260-270, and the alteration of this T cell epitope by posttranslational modifications is known to be critical for development of arthritis in mice. Using CII-specific T cell hybridomas we have now shown that the immunodominant T cell epitope in the normal (healthy) human and rat joint cartilage is O-glycosylated at the critical T cell receptor recognition position 264 with a mono- or di-saccharide attached to a hydroxylysine. In contrast, in the arthritic human and rat joint cartilage there are both glycosylated and non-glycosylated CII forms. Glycosylated CII from normal cartilage could not be recognized by T cells reactive to peptides having only lysine or hydroxylysine at position 264, showing that antigen-presenting cells could not degrade the O-linked carbohydrate. Thus, the variable forms of the glycosylated epitope are determined by the structures present in cartilage, and these vary during the disease course. We conclude that the chondrocyte determines the structures presented to the immune system and that these structures are different in normal versus arthritic states.

Published
2005
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