Publication

The Hochberg: Rheumatology, 7e: Biology and immunopathogenesis of vasculitis Elisabeth Brouwer • Peter Heeringa • Cees G.M. Kallenberg

Brouwer, E., Heeringa, P. & Kallenberg, C. G. M., 1-Mar-2018, Hochberg: Rheumatology . Weinblatt, M.D., M. E. (ed.). Boston: Elsevier, Vol. 7th . p. 162-1-162-9 9 p.

Research output: Chapter in Book/Report/Conference proceedingChapterAcademic

Key Points
■ The interplay between leukocytes and endothelium is important in inflammatory
processes in general and in the pathogenesis of vasculitis in particular.
■ Cytokine-induced endothelial cell activation and leukocyte–endothelium interactions
are coordinated processes underlying differential leukocyte recruitment to sites of
inflammation
■ Immune complex formation and deposition underlie the small-vessel vasculitides in
immunoglobulin A vasculitis (Henoch-Schönlein purpura), anti–glomerular basement
membrane disease, cryoglobulinemic vasculitis, and hypocomplementemic urticarial
vasculitis.
■ Clinical and experimental data suggest but do not prove that antineutrophil
cytoplasmic antibodies (ANCAs) directed against proteinase 3, and myeloperoxidase
are pathogenic in the ANCA-associated small-vessel vasculitides.
■ Toll-like receptor–mediated dendritic cell activation in the adventitia followed by
interferon-γ–producing T helper cell 1 and interleukin-17–producing T helper cell 17
responses to as yet undefined antigen(s) is the major pathogenic event in the
medium- and large-vessel vasculitides
Original languageEnglish
Title of host publicationHochberg
Subtitle of host publicationRheumatology
EditorsMichael E. Weinblatt, M.D.
Place of PublicationBoston
PublisherElsevier
ChapterChapter 162
Pages162-1-162-9
Number of pages9
Volume7th
Publication statusPublished - 1-Mar-2018

    Keywords

  • vasculitis

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