Expression of the β chemokines CCL3, CCL4, CCL5 and their receptors in idiopathic inflammatory myopathies

被引:47
作者
Civatte, M
Bartoli, C
Schleinitz, N
Chetaille, B
Pellissier, JF
Figarella-Branger, D
机构
[1] Univ Mediterranee, Fac Med Timone, Lab Biopathol Nerveuse & Musculaire EA 3281, IPHM,IFR 125, F-13385 Marseille 05, France
[2] Hop Enfants La Timone, Assistance Publ Hosp Marseille, Serv Anat Pathol, Marseille, France
关键词
chemokines; inflammatory myopathies; receptors;
D O I
10.1111/j.1365-2990.2004.00591.x
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
The idiopathic inflammatory myopathies (IIM) are a group of autoimmune diseases characterized by chronic lymphocytic and macrophagic infiltration in muscle. Because the mechanism for recruitment of these cells probably involves chemokines, we focused on the study of the expression pattern of some beta chemokines and receptors because it may provide a basis for selective immunotherapy. The expression of CCL3 (MIP-1alpha), CCL4 (MIP-1beta), CCL5 (RANTES) and their main receptors (CCR1 and CCR5) was studied by semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR) and immunohistochemistry in a series of 16 IIM and five controls (four normal muscles and one tonsil). Except for CCL5, strong expression was observed by RT-PCR with all molecules in all IIM subtypes in comparison to control muscle. Immunohistochemistry revealed diffuse CCL4 expression in all vessels in dermatomyositis. In both polymyositis and sporadic inclusion body myositis (s-IBM) it was restricted to vessels in the vicinity of inflammatory exudates. CCL5 expression was low, restricted to a few inflammatory cells in all IIM; CCR1 expression was mainly restricted to macrophages and s-IBM endothelial cells, whereas CCR5 was localized in inflammatory cells invading non-necrotic muscle fibres. Expressions of both receptors were also recorded in few muscle fibres. In conclusion, the upregulation of beta chemokines and receptors in IIM and their differential expression by various cells may contribute to chronic inflammation and to the peculiar distribution of inflammatory exudates in these diseases.
引用
收藏
页码:70 / 79
页数:10
相关论文
共 44 条
  • [1] Adams EM, 1997, P ASSOC AM PHYSICIAN, V109, P275
  • [2] Askanas V, 2001, J NEUROPATH EXP NEUR, V60, P1
  • [3] Bartoli C, 2001, ACTA NEUROPATHOL, V102, P385
  • [4] POLYMYOSITIS AND DERMATOMYOSITIS .1.
    BOHAN, A
    PETER, JB
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 1975, 292 (07) : 344 - 347
  • [5] Increased expression of β-chemokines in muscle of patients with inflammatory myopathies
    Confalonieri, P
    Bernasconi, P
    Megna, P
    Galbiati, S
    Cornelio, F
    Mantegazza, R
    [J]. JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 2000, 59 (02) : 164 - 169
  • [6] Dalakas Marinos C., 2001, Current Opinion in Pharmacology, V1, P300, DOI 10.1016/S1471-4892(01)00053-4
  • [7] De Bleecker JL, 2002, J NEUROL SCI, V199, pS4
  • [8] Differential expression of chemokines in inflammatory myopathies
    De Bleecker, JL
    De Paepe, B
    Vanwalleghem, IE
    Schröder, JM
    [J]. NEUROLOGY, 2002, 58 (12) : 1779 - 1785
  • [9] Cytokines and chemokines are both expressed by human myoblasts: possible relevance for the immune pathogenesis of muscle inflammation.
    De Rossi, M
    Bernasconi, P
    Baggi, F
    Malefyt, RD
    Mantegazza, R
    [J]. INTERNATIONAL IMMUNOLOGY, 2000, 12 (09) : 1329 - 1335
  • [10] EXPRESSION OF CELL-ADHESION MOLECULES IN INFLAMMATORY MYOPATHIES AND DUCHENNE DYSTROPHY
    DEBLEECKER, JL
    ENGEL, AG
    [J]. JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1994, 53 (04) : 369 - 376