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Complement activation by both classical and alternative pathways is critical for the effector phase of arthritis.

Hietala, Max Albert, 1969 (author)
Gothenburg University,Göteborgs universitet,Institutionen för medicinsk och fysiologisk kemi,Institute of Medical Biochemistry,Göteborg University, Göteborg, Sweden
Nandakumar, Kutty Selva, 1965- (author)
Lund University, Lund, Sweden
Persson, Linda, 1971 (author)
Gothenburg University,Göteborgs universitet,Institutionen för medicinsk och fysiologisk kemi,Institute of Medical Biochemistry,Göteborg University, Göteborg, Sweden
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Fahlén, Susann (author)
Gothenburg University,Göteborgs universitet,Institutionen för medicinsk och fysiologisk kemi,Institute of Medical Biochemistry,Göteborg University, Göteborg, Sweden
Holmdahl, Rikard (author)
Lund University,Lunds universitet,Immunologi,Forskargrupper vid Lunds universitet,Immunology,Lund University Research Groups,Lund University, Lund, Sweden
Pekna, Marcela, 1966 (author)
Gothenburg University,Göteborgs universitet,Institutionen för medicinsk och fysiologisk kemi,Institute of Medical Biochemistry,Göteborg University, Göteborg, Sweden
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 (creator_code:org_t)
Wiley, 2004
2004
English.
In: European journal of immunology. - : Wiley. - 0014-2980 .- 1521-4141. ; 34:4, s. 1208-16
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • To analyze the role of the classical and alternative pathways of complement activation in the effector phase of arthritis, we have induced arthritis in C3- and factor B (FB)-deficient (C3(-/-) and FB(-/-)) DBA/1J mice using well-defined monoclonal IgG2b and IgG2a antibodies to type II collagen. In control DBA/1J mice, severe swelling of the joints, destruction of cartilage and erosion of bone developed very rapidly with a 100% incidence and a peak on days 7-10. Although 75% of C3(-/-) mice developed arthritis, the clinical severity was very mild and the onset was delayed. Severity of arthritis in FB(-/-) mice ranked intermediate in comparison with C3(-/-) and control mice with an incidence of 100%. Immunohistochemical analysis of the inflamed joints demonstrated substantial reduction in macrophage and neutrophilic leukocyte infiltration in both C3(-/-) and FB(-/-) mice, thereby confirming the clinical findings. We conclude that both the classical and the alternative pathways of complement activation are involved in the effector phase of arthritis.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Immunologi inom det medicinska området (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Immunology in the medical area (hsv//eng)
MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Reumatologi och inflammation (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Rheumatology and Autoimmunity (hsv//eng)

Keyword

Animals
Arthritis
Experimental
immunology
pathology
Complement Activation
immunology
Complement C3
deficiency
Complement Factor B
deficiency
Complement Pathway
Alternative
Complement Pathway
Classical
Enzyme-Linked Immunosorbent Assay
Immunohistochemistry
Inflammation
immunology
pathology
Joints
pathology
Male
Mice
Mice
Knockout
Monocytes
immunology
pathology
Neutrophils
immunology
pathology
rodent
complement
rheumatoid arthritis
transgenic
knockout
Animals

Publication and Content Type

ref (subject category)
art (subject category)

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