Effector lymphocytes in autoimmunity

Curr Opin Immunol. 2001 Dec;13(6):663-9. doi: 10.1016/s0952-7915(01)00276-x.


Autoimmune diseases result from complex interactions among different T- and B-lymphocyte subpopulations that target a rapidly growing number of autoantigens on different cell types. The etiology of most spontaneous autoimmune disorders, and both the kinetics and hierarchy of the underlying autoimmune responses are poorly understood. However, important advances have been made in recent years in our understanding of how autoreactive lymphocytes cause tissue damage, including the discovery that granzyme B binds to a cell surface receptor on target cells. This review is an attempt to summarize recent developments in this area.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Apoptosis Regulatory Proteins
  • Autoimmune Diseases / immunology*
  • Autoimmunity*
  • B-Lymphocytes / immunology*
  • Cytokines / physiology
  • Diabetes Mellitus, Type 1 / immunology
  • Granzymes
  • Membrane Glycoproteins / physiology
  • Mice
  • Models, Immunological
  • Secretory Vesicles / metabolism
  • Serine Endopeptidases / metabolism
  • T-Lymphocytes / immunology*
  • T-Lymphocytes, Cytotoxic / immunology*
  • TNF-Related Apoptosis-Inducing Ligand
  • Tumor Necrosis Factor-alpha / physiology
  • fas Receptor / metabolism


  • Apoptosis Regulatory Proteins
  • Cytokines
  • Membrane Glycoproteins
  • TNF-Related Apoptosis-Inducing Ligand
  • Tnfsf10 protein, mouse
  • Tumor Necrosis Factor-alpha
  • fas Receptor
  • Granzymes
  • Gzmb protein, mouse
  • Serine Endopeptidases