Autoantibodies produced at the site of tissue damage provide evidence of humoral autoimmunity in inclusion body myositis.

Autoantibodies produced at the site of tissue damage provide evidence of humoral autoimmunity in inclusion body myositis.
复制标题

DOI:
10.1371/journal.pone.0046709
复制
发表时间:
2012
期刊:
影响因子:
3.7
通讯作者:
O'Connor KC
O'Connor KC
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Ray A;Amato AA;Bradshaw EM;Felice KJ;DiCapua DB;Goldstein JM;Lundberg IE;Nowak RJ;Ploegh HL;Spooner E;Wu Q;Willis SN;O'Connor KC

文献摘要

参考文献

相似文献

Inclusion body myositis (IBM) belongs to a group of muscle diseases known as the inflammatory myopathies. The presence of antibody-secreting plasma cells in IBM muscle implicates the humoral immune response in this disease. However, whether the humoral immune response actively contributes to IBM pathology has not been established. We sought to investigate whether the humoral immune response in IBM both in the periphery and at the site of tissue damage was directed towards self-antigens. Peripheral autoantibodies present in IBM serum but not control serum recognized self-antigens in both muscle tissue and human-derived cell lines. To study the humoral immune response at the site of tissue damage in IBM patients, we isolated single plasma cells directly from IBM-derived muscle tissue sections and from these cells, reconstructed a series of recombinant immunoglobulins (rIgG). These rIgG, each representing a single muscle-associated plasma cell, were examined for reactivity to self-antigens. Both, flow cytometry and immunoblotting revealed that these rIgG recognized antigens expressed by cell lines and in muscle tissue homogenates. Using a mass spectrometry-based approach, Desmin, a major intermediate filament protein, expressed abundantly in muscle tissue, was identified as the target of one IBM muscle-derived rIgG. Collectively, these data support the view that IBM includes a humoral immune response in both the periphery and at the site of tissue damage that is directed towards self-antigens.
DOI: 10.1136/ard.60.2.116
发表时间: 2001-02-01
影响因子: 27.4
作者:
Brouwer, R;Hengstman, GJD;van Venrooij, WJ
通讯作者: van Venrooij, WJ
DOI: 10.1136/ard.2008.091405
发表时间: 2009-06-01
影响因子: 27.4
作者:
Krystufkova, O.;Vallerskog, T.;Lundberg, I. E.
通讯作者: Lundberg, I. E.
DOI: 10.1093/rheumatology/ker088
发表时间: 2011-12-01
期刊: RHEUMATOLOGY
影响因子: 5.5
作者:
Mahler, Elien A. M.;Blom, Marlies;Vonk, Madelon C.
通讯作者: Vonk, Madelon C.
DOI: 10.1007/s11926-010-0102-5
发表时间: 2010-06
影响因子: 5
作者:
Greenberg, Steven A
通讯作者: Greenberg, Steven A
DOI: 10.1371/journal.pone.0020266
发表时间: 2011
期刊: PloS one
影响因子: 3.7
作者:
Salajegheh M;Lam T;Greenberg SA
通讯作者: Greenberg SA