Transfer of experimental glomerulonephritis in chickens by mononuclear cells

Abstract

We have produced experimental autoimmune glomerulonephritis (EAG) in histocompatible SC chickens by immunization with different types of glomerular antigen. The development of EAG was time, but not antigen, dependent. Transfer of mononuclear cells from spleens and kidneys of nephritic animals resulted in EAG in naive recipients. Transferred EAG developed earlier than in immunized donors and was not associated with circulating or bound anti-GBM antibodies. Control recipients did not develop disease from control cells alone, soluble antigen, or antigen plus control cells. The cells which transferred EAG appeared morphologically by light and electron microscopy to be lymphocytes, sedimented as lymphocytes, were positive with anti-serum to thymocytes but negative with anti-bursa anti-serum, stained as T-cells with monoclonal antibodies and underwent blast transformation in response to mitogen and GBM antigen. Other organ specific diseases have been transferred by cells alone; to our knowledge this is the first description of glomerulonephritis transferred by cells alone. This new pathogenetic process may play an important role in the development of glomerulonephritis in other animal models as well as in humans.

Effector CD4+ T cells recognize intravascular antigen presented by patrolling monocytes

“…In addition to humoral mediators, CD4 + T cells also have an important function in the development of glomerular injury and dysfunction in severe, rapidly progressive forms of glomerulonephritis. Intraglomerular T cells are detectable in humans with rapidly progressive glomerulonephritis 19 – 21 , and functional studies in animal models demonstrate that disease-inducing effector responses can be directed by CD4 + T cells responding to antigen located intravascularly within the glomerulus 15 , 16 , 22 – 24 .…”