Pathology and immunology of lupus glomerulonephritis: can we bridge the two?
Aberrant immune responses underwrite lupus glomerulonephritis and may contribute to glomerular cell proliferation and inflammation. Recent studies provide evidence that apoptotic immune cells may initiate immune events leading to tissue damage. Nucleosomes within apoptotic particles are recognized by B cells and other antigen presenting cells and represent the most likely inciting antigen for autoantibody production. Some of these antibodies are nephritogenic depending on fine structural composition and antigen recognition in the circulation or on renal cells. Deficient complement components contribute to reduced clearance of circulating and native kidney apoptotic cells. This review summarizes current concepts in lupus immune pathogenesis and attempts to bridge immunology to pathology of lupus glomerulonephritis.
Liapis
Helen
H
Department of Pathology and Immunology, Division of Anatomic and Molecular Pathology, Washington University School of Medicine, 660 South Euclid Avenue Campus, 8118, St Louis, MO 63110, USA. liapis@path.wustl.edu
Tsokos
George C
GC
D000818:Animals; D000917:Antibody Formation / Q000276:immunology; D017209:Apoptosis; D001323:Autoantibodies / Q000276:immunology; D049109:Cell Proliferation; D003165:Complement System Proteins / Q000276:immunology; D006801:Humans; D008181:Lupus Nephritis / Q000276:immunology* / Q000473:pathology*
D001323:Autoantibodies; D003165:Complement System Proteins