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Sökning: id:"swepub:oai:DiVA.org:hh-48815" > 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

Nandakumar, Kutty Selva, 1965- (författare)
Lund University,Lunds universitet,Immunologi,Forskargrupper vid Lunds universitet,Immunology,Lund University Research Groups,Lund University, Lund, Sweden
Bäcklund, Johan (författare)
Lund University,Lunds universitet,Immunologi,Forskargrupper vid Lunds universitet,Immunology,Lund University Research Groups,Lund University, Lund, Sweden
Vestberg, Mikael (författare)
Lund University,Lunds universitet,Immunologi,Forskargrupper vid Lunds universitet,Immunology,Lund University Research Groups,Lund University, Lund, Sweden
visa fler...
Holmdahl, Rikard (författare)
Lund University,Lunds universitet,Immunologi,Forskargrupper vid Lunds universitet,Immunology,Lund University Research Groups,Lund University, Lund, Sweden
visa färre...
 (creator_code:org_t)
Springer Science and Business Media LLC, 2004
2004
Engelska.
Ingår i: Arthritis Research & Therapy. - : Springer Science and Business Media LLC. - 1478-6362 .- 1465-9905. ; 6:6
  • Tidskriftsartikel (refereegranskat)
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

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