Vasculitis of small blood vessels - some riddles about IgA and about the complexity of transmigration

被引:11
作者
Sunderkoetter, Cord [1 ,2 ]
机构
[1] Univ Munster, Dept Dermatol, D-48149 Munster, Germany
[2] Univ Munster, Inst Immunol, D-48149 Munster, Germany
关键词
glycosylation; Henoch -Schoenlein purpura; IgA; leukocytoclastic; mouse model; transmigration; vasculitis; HENOCH-SCHONLEIN PURPURA; CIRCULATING IMMUNE-COMPLEXES; LEUKOCYTOCLASTIC VASCULITIS; HYPERSENSITIVITY VASCULITIS; ABERRANT GLYCOSYLATION; HUMAN-NEUTROPHILS; NEPHROPATHY; ADULTS; SKIN; CLASSIFICATION;
D O I
10.1111/j.1600-0625.2008.00791.x
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
Research on leukocytoclastic vasculitis (LcV) provides insights into mechanisms of antibody-mediated immune responses as well as into the complex process of neutrophil transmigration. Clinical observations on immune complex vasculitis have revealed that adult patients with IgA containing immune complexes [Henoch-Schoenlein purpura (HSP)] have a higher rate of severe complications than children with HSP or adult patients with IgG or IgM containing immune complexes. This has direct impact on classification and management of vasculitis and warrants further studies on pathophysiology of IgA and on aberrant glycosylation of IgA1 associated with renal involvement. In order to dissect the pathomechanisms specific for LcV, we have been comparing different mouse models of LcV with a nonvasculitic, acute inflammation (i.e. irritant contact dermatitis). We found that one characteristic constellation in the vasculitis models encompasses interference with both normal transmigration and activation of neutrophils. Toxic products released by activated neutrophils have the potential to damage endothelial cells. However, one still needs to reveal how exactly they exert such damaging effects during diapedesis in vivo, considering the short contacts between neutrophils and endothelial cells. This review shows that research on LcV is embedded in an exciting context revealing special features of transmigration and antibody-mediated immune responses.
引用
收藏
页码:91 / 96
页数:6
相关论文
共 49 条
  • [1] Abnormal IgA glycosylation in Henoch-Schonlein purpura restricted to patients with clinical nephritis
    Allen, AC
    Willis, FR
    Beattie, TJ
    Feehally, J
    [J]. NEPHROLOGY DIALYSIS TRANSPLANTATION, 1998, 13 (04) : 930 - 934
  • [2] Treatment of Antineutrophil cytoplasmic antibody-associated vasculitis - A systematic review
    Bosch, Xavier
    Guilabert, Antonio
    Espinosa, Gerard
    Mirapeix, Eduard
    [J]. JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2007, 298 (06): : 655 - 669
  • [3] B-cell O-galactosyltransferase activity, and expression of O-glycosylation genes in bone marrow in IgA nephropathy
    Buck, K. S.
    Smith, A. C.
    Molyneux, K.
    El-Barbary, H.
    Feehally, J.
    Barratt, J.
    [J]. KIDNEY INTERNATIONAL, 2008, 73 (10) : 1128 - 1136
  • [4] Cutaneous vasculitis: a review
    Crowson, AN
    Mihm, MC
    Magro, CM
    [J]. JOURNAL OF CUTANEOUS PATHOLOGY, 2003, 30 (03) : 161 - 173
  • [5] Immunoglobulin A-associated lymphocytic vasculopathy: a clinicopathologic study of eight patients
    Crowson, AN
    Magro, CM
    Usmani, A
    McNutt, NS
    [J]. JOURNAL OF CUTANEOUS PATHOLOGY, 2002, 29 (10) : 596 - 601
  • [6] CUTANEOUS WEGENERS GRANULOMATOSIS - CLINICAL, HISTOPATHOLOGIC, AND IMMUNOPATHOLOGIC FEATURES OF 30 PATIENTS
    DAOUD, MS
    GIBSON, LE
    DEREMEE, RA
    SPECKS, U
    ELAZHARY, RA
    SU, WPD
    [J]. JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY, 1994, 31 (04) : 605 - 612
  • [7] IgA1 glycosylation in IgA nephropathy: As sweet as it can be
    Eijgenraam, J. W.
    van Kooten, C.
    [J]. KIDNEY INTERNATIONAL, 2008, 73 (10) : 1106 - 1108
  • [8] FLIGIEL SEG, 1984, AM J PATHOL, V115, P375
  • [9] FLIGIEL SEG, 1984, AM J PATHOL, V115, P418
  • [10] Comparative clinical and epidemiological study of hypersensitivity vasculitis versus Henoch-Schonlein purpura in adults
    García-Porrúa, C
    González-Gay, MA
    [J]. SEMINARS IN ARTHRITIS AND RHEUMATISM, 1999, 28 (06) : 404 - 412