Intravenous immunoglobulin (IVIG) therapy acts independently of the neonatal Fc-receptor in experimental epidermolysis bullosa acquisita

被引：0
|
作者：
Kasperkiewicz, M. [1 ]
Ishii, N. [1 ]
Hirose, M. [1 ]
Freitag, M. [1 ]
Schmidt, E. [1 ]
Recke, A. [1 ]
Zillikens, D. [1 ]
Ludwig, R. J. [1 ]
机构：
[1] Med Univ Lubeck, Klin Dermatol Allergol & Venerol, D-23538 Lubeck, Germany
来源：
EXPERIMENTAL DERMATOLOGY | 2009年 / 18卷 / 03期
关键词：
D O I：
暂无
中图分类号：
R75 [皮肤病学与性病学];
学科分类号：
100206 ;
摘要：
引用
收藏
页码：290 / 290
页数：1
相关论文
共 44 条
  • [21] Blocking the interaction with complement and Fc receptors abolishes antibody-induced blistering in experimental epidermolysis bullosa acquisita
    Sesarman, A. V.
    Mihai, S.
    Chiriac, M. T.
    Olaru, F.
    Thurman, J. M.
    Zillikens, D.
    Sitaru, C.
    EXPERIMENTAL DERMATOLOGY, 2007, 16 (03) : 223 - 223
  • [22] C5aR2 Deficiency Ameliorates Inflammation in Murine Epidermolysis Bullosa Acquisita by Regulating Fc? Receptor Expression on Neutrophils
    Seiler, Daniel Leonard
    Kleingarn, Marie
    Kahler, Katja Hendrika
    Gruner, Caroline
    Schanzenbacher, Jovan
    Ehlers-Jeske, Elvira
    Kenno, Samyr
    Sadik, Christian David
    Schmidt, Enno
    Bieber, Katja
    Kohl, Jorg
    Ludwig, Ralf J.
    Karsten, Christian Marcel
    JOURNAL OF INVESTIGATIVE DERMATOLOGY, 2022, 142 (10) : 2715 - +
  • [23] Intravenous immunoglobulin (IVIg) acts directly on conventional T cells to suppress T cell receptor signaling
    Hori, Ayane
    Fujimura, Takashi
    Murakami, Mai
    Park, Jungyeon
    Kawamoto, Seiji
    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2020, 522 (03) : 792 - 798
  • [24] Neonatal Fc receptor induces intravenous immunoglobulin growth suppression in Langerhans cell histiocytosis
    Nabeshima, Yuka
    Kataoka, Tatsuki R.
    Ueshima, Chiyuki
    Saito, Narumi
    Hirata, Masahiro
    Takeuchi, Yasuhide
    Takei, Yusuke
    Moriyoshi, Koki
    Ono, Kazuo
    Haga, Hironori
    PATHOLOGY INTERNATIONAL, 2021, 71 (03) : 191 - 198
  • [25] Failure of intravenous immunoglobulin (IVIg) therapy in experimental autoimmune neuritis (EAN) of the Lewis rat
    Enders, U
    Toyka, KV
    Hartung, HP
    Gold, R
    JOURNAL OF NEUROIMMUNOLOGY, 1997, 76 (1-2) : 112 - 116
  • [26] Fc gamma receptor IIB (FcγRIIB)-dependent negative feedback is not involved in the in vitro inhibition of IgE production by intravenous:: Immunoglobulin (IVIG)
    Mazer, B
    Zhuang, Q
    Millette, R
    Fixman, E
    JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2000, 105 (01) : S178 - S179
  • [27] Treatment of epidermolysis bullosa acquisita with intravenous immunoglobulin in patients non-responsive to conventional therapy: clinical outcome and post-treatment long-term follow-up
    Ahmed, A. R.
    Guercan, H. M.
    JOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY AND VENEREOLOGY, 2012, 26 (09) : 1074 - 1083
  • [28] The retinoid-related orphan receptor alpha is essential for the end-stage effector phase of experimental epidermolysis bullosa acquisita
    Sadeghi, Hengameh
    Gupta, Yask
    Moeller, Steffen
    Samavedam, Unni K.
    Behnen, Martina
    Kasprick, Anika
    Bieber, Katja
    Mueller, Susen
    Kalies, Kathrin
    Marques, Andreia de Castro
    Recke, Andreas
    Schmidt, Enno
    Zillikens, Detlef
    Laskay, Tamas
    Mariani, Jean
    Ibrahim, Saleh M.
    Ludwig, Ralf J.
    JOURNAL OF PATHOLOGY, 2015, 237 (01): : 111 - 122
  • [29] The retinoid-related orphan receptor alpha is essential for the end-stage effector phase of experimental epidermolysis bullosa acquisita
    Sadeghi, H.
    Gupta, Y.
    Moeller, S.
    Samavedam, U. K.
    Behnen, M.
    Mueller, S.
    Kalies, K.
    Marques, A. de Castro
    Recke, A.
    Schmidt, E.
    Zillikens, D.
    Laskay, T.
    Mariani, J.
    Ibrahim, S.
    Ludwig, R. J.
    EXPERIMENTAL DERMATOLOGY, 2015, 24 (03) : E24 - E24
  • [30] IgG Fc receptor polymorphisms in human disease: Implications for intravenous immunoglobulin therapy
    Binstadt, BA
    Geha, RS
    Bonilla, FA
    JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2003, 111 (04) : 697 - 703
12345