Biomedical subjects

N M van Sorge

Publications and source records attributed to N M van Sorge.

3 recordsLinked to original sources

PubMed2004

Pathogenicity of anti-ganglioside antibodies in the Guillain-Barré syndrome.

Guillain-Barré syndrome (GBS) is a postinfectious inflammatory polyradiculo-neuropathy characterized by flaccid paralysis. Antibodies directed against glycolipid structures (gangliosides), which are highly expressed in the peripheral nervous system, are frequently detected in sera from GBS patients. These antibodies interfere with nerve conduction and have been shown to activate phagocytes via IgG receptors (FcgammaR). These findings support an important role of glycolipid-specific antibodies in the pathogenesis of GBS.

Antibodies↗

PubMed2003

FcgammaR polymorphisms: Implications for function, disease susceptibility and immunotherapy.

Leukocyte Fcgamma receptors (FcgammaR) confer potent cellular effector functions to the specificity of IgG. FcgammaR-induced leukocyte functions, including antibody-dependent cellular cytotoxicity, phagocytosis, superoxide generation, degranulation, cytokine production and regulation of antibody production, are essential for host defense and immune regulation. The efficacy of IgG-induced FcgammaR function displays inter-individual heterogeneity due to genetic polymorphisms of three FcgammaR subclasses, FcgammaRIIa (CD32a), FcgammaRIIIa (CD16a), and FcgammaRIIIb (CD16b). FcgammaR polymorphisms have been associated with infectious and autoimmune disease, or with disease severity. FcgammaR polymorphisms may furthermore serve as markers for therapeutic efficacy and side-effects of treatment with monoclonal antibodies. In this review, FcgammaR function and the relevance of FcgammaR polymorphisms as prognostic markers for inflammatory disease and antibody-based immunotherapy are discussed.

Autoimmune Diseases↗

PubMed1999

Effective phagocytosis and killing of Candida albicans via targeting FcgammaRI (CD64) or FcalphaRI (CD89) on neutrophils.

Invasive fungal infections are an increasing problem for immunocompromised patients. As an approach to improve targeting of polymorphonuclear leukocytes (PMNL) toward Candida albicans, the effect of bispecific antibodies (BsAbs) directed against C. albicans and either FcalphaRI or FcgammaRI was evaluated. Control PMNL and in vivo granulocyte colony-stimulating factor (G-CSF)-primed PMNL served as effector cells. A new radiometric killing assay for measuring candidacidal activity was developed to facilitate quantification of PMNL-mediated killing of C. albicans. BsAbs directed to either FcgammaRI (CD64) or FcalphaRI (CD89) on human PMNL effectively enhanced both phagocytosis and killing of C. albicans in vitro. Fungicidal activity triggered via FcgammaRI required in vivo priming with G-CSF, whereas FcalphaRI-mediated activity was not dependent on this growth factor. Furthermore, PMNL from human FcgammaRI-transgenic mice effectively phagocytosed and eliminated C. albicans in the presence of BsAbs. These results document the capacity of FcR-directed BsAbs and G-CSF to trigger antifungal immune responses.

Animals↗