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Collagen type II (C...
Collagen type II (CII)-specific antibodies induce arthritis in the absence of T or B cells but the arthritis progression is enhanced by CII-reactive T cells
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- Nandakumar, Kutty Selva, 1965- (författare)
- Lund University,Lunds universitet,Immunologi,Forskargrupper vid Lunds universitet,Immunology,Lund University Research Groups,Lund University, Lund, Sweden
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- Bäcklund, Johan (författare)
- Lund University,Lunds universitet,Immunologi,Forskargrupper vid Lunds universitet,Immunology,Lund University Research Groups,Lund University, Lund, Sweden
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- Vestberg, Mikael (författare)
- Lund University,Lunds universitet,Immunologi,Forskargrupper vid Lunds universitet,Immunology,Lund University Research Groups,Lund University, Lund, Sweden
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- Holmdahl, Rikard (författare)
- Lund University,Lunds universitet,Immunologi,Forskargrupper vid Lunds universitet,Immunology,Lund University Research Groups,Lund University, Lund, Sweden
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(creator_code:org_t)
- Springer Science and Business Media LLC, 2004
- 2004
- Engelska.
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Ingår i: Arthritis Research & Therapy. - : Springer Science and Business Media LLC. - 1478-6362 .- 1465-9905. ; 6:6
- Relaterad länk:
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https://doi.org/10.1...
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https://arthritis-re...
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https://portal.resea... (primary) (free)
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http://dx.doi.org/10... (free)
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https://urn.kb.se/re...
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https://doi.org/10.1...
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https://lup.lub.lu.s...
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Abstract
Ämnesord
Stäng
- Antibodies against type II collagen (anti-CII) are arthritogenic and have a crucial role in the initiation of collagen-induced arthritis. Here, we have determined the dependence of T and B cells in collagen-antibody-induced arthritis (CAIA) during different phases of arthritis. Mice deficient for B and/or T cells were susceptible to the CAIA, showing that the antibodies induce arthritis even in the absence of an adaptive immune system. To determine whether CII-reactive T cells could have a role in enhancing arthritis development at the effector level of arthritis pathogenesis, we established a T cell line reactive with CII. This T cell line was oligoclonal and responded to different post-translational forms of the major CII epitope at position 260-270 bound to the Aq class II molecule. Importantly, it cross-reacted with the mouse peptide although it is bound with lower affinity to the Aq molecule than the corresponding rat peptide. The T cell line could not induce clinical arthritis per se in Aq-expressing mice even if these mice expressed the major heterologous CII epitope in cartilage, as in the transgenic MMC (mutated mouse collagen) mouse. However, a combined treatment with anti-CII monoclonal antibodies and CII-reactive T cells enhanced the progression of severe arthritis.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Reumatologi och inflammation (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Rheumatology and Autoimmunity (hsv//eng)
Nyckelord
- Adoptive Transfer
- Animals
- Antibodies
- Monoclonal/immunology/*toxicity
- Antibody Specificity
- Arthritis
- Experimental/*immunology
- B-Lymphocytes/immunology
- Collagen Type II/chemistry/*immunology
- Crosses
- Genetic
- Disease Progression
- Epitopes
- T-Lymphocyte/*immunology
- Female
- Glycosylation
- Histocompatibility Antigens Class II/immunology
- Immunity
- Cellular
- Immunization
- Passive
- Immunologic Deficiency Syndromes/immunology
- Male
- Mice
- Mice
- Inbred C3H/immunology
- Mice
- Inbred C57BL
- Mice
- Inbred DBA
- Mice
- Knockout
- Protein Processing
- Post-Translational
- Rats
- Receptors
- Antigen
- T-Cell
- alpha-beta/deficiency
- T-Lymphocyte Subsets/*immunology
- T cells
- monoclonal antibodies
- collagen type II
- arthritis
- B cells
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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