Induction of Fc receptors for IgA on murine T cell hybridoma by human monoclonal IgA and by high molecular weight IgA in IgA nephropathy
Chevailler, A.; Monteiro, R.C.; Daëron, M.; Lesavre, P.
Clinical and Experimental Immunology 67(1): 114-123
1987
ISSN/ISBN: 0009-9104 PMID: 3497739 Document Number: 293028
A reproducible immunocyto-adherence assay has been developed to study the modulation of Fc receptors for IgA (Fc.alpha.R), using a murine T cell hybridoma (T2D4), which expresses Fc receptors for all known isotypes of secreted immunoglobulins. By using sheep red blood cells coated with the hapten 2-4-6 trinitrophenyl (TNP), as indicator cells, and a murine monoclonal IgA (MOPC 315) antibody with anti-TNP activity, we were able to study the Fc.alpha.R on T2D4 cells. We found that: (a) murine Fc.alpha.R can bind human monoclonal IgA, and this binding is isotype specific since it was inhibited by human monoclonal IgA but not by human monoclonal IgG or IgM; (b) the expression of murine Fc.alpha.R is inducible by human monoclonal IgA, and this effect is isotype specific since it is not observed with human monoclonal IgM or IgG (c) sera from patients with IgA nephrectomy can also induce Fc.alpha.R expression: by contrast, no induction was observed with normal human sera, (d) in one serum from an IgA-nephropathy patient, the inducer factor was characterized by affinity chromatography on anti-IgA-Sepharose and by gel filtration: high molecular weight IgA, probably IgA aggregates or immune complexes were recognized to be responsible for the induction of murine Fc.alpha.R expression.