Lymphocytes, cytokines, inflammation, and immune trafficking.
Studies that were published over the past year have added new knowledge to our understanding of cellular abnormalities in systemic lupus erythematosus (SLE). Antigen-specific and "pathogenic" T cells can be identified and characterized in SLE. Interleukin-10 has been added to the factors that may promote B cell overactivity and autoantibody production. Protein kinase isozyme I was shown to be deficient in patients with SLE, indicating defects in cell signaling events. Aberrant expression of adhesion molecules on the surface membrane of leukocytes and endothelial cells was shown, with important mechanistic and therapeutic implications. Disruption of the lymphokine network (anti-interleukin-10 antibody) and the function of adhesion-costimulatory molecules (CTLA-4-immunoglobulin) were shown to be therapeutically significant in murine SLE.
Tsokos
G C
GC
Department of Clinical Physiology, Walter Reed Army Institute of Research, Washington, DC 20307-5100, USA.
D017209:Apoptosis; D001402:B-Lymphocytes / Q000502:physiology; D016207:Cytokines / Q000502:physiology*; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D008180:Lupus Erythematosus, Systemic / Q000276:immunology* / Q000503:physiopathology*; D008214:Lymphocytes / Q000502:physiology*; D008222:Lymphokines / Q000502:physiology; D013601:T-Lymphocytes / Q000502:physiology
D016207:Cytokines; D008222:Lymphokines