Prevention of B cell clonal deletion and anergy by activated T cells and their lymphokines.
B cell tolerance is described as the absence of a measurable antibody forming response to an antigenic challenge. The establishment of antigen-specific tolerance requires, by definition, engagement of the B cell antigen-specific receptor. However, only in some circumstances does this engagement lead to tolerance, while in others it produces B cell activation and secretion of immunoglobulins. Several mechanisms occur naturally in vivo abrogating the expression of deleterious autoantibodies and contributing to the state of self-tolerance. In this review, we will examine different ways in which B cell tolerance can be broken, focusing on evidence showing that activated-T cells and/or their lymphokines can prevent B cell clonal deletion and thus have a potential role in the pathogenesis of autoimmune diseases. This approach is based on the well-known association of several lymphokines, such as IL-1, IL-2, IL-4, IL-5, and type I interferons, with autoimmune phenomena in vivo.
Alés-Martínez
J E
JE
Centro de Biología Molecular, Universidad Autónoma de Madrid, Spain.
Cuende
E
E
Gaur
A
A
Scott
D W
DW
D000818:Animals; D015551:Autoimmunity; D016175:B-Lymphocyte Subsets / Q000166:cytology* / Q000187:drug effects / Q000276:immunology; D002999:Clone Cells / Q000276:immunology; D006801:Humans; D007108:Immune Tolerance; D016219:Immunotherapy, Adoptive; D008213:Lymphocyte Activation; D008222:Lymphokines / Q000502:physiology*; D008223:Lymphoma / Q000473:pathology; D051379:Mice; D008954:Models, Biological; D015398:Signal Transduction; D016176:T-Lymphocyte Subsets / Q000276:immunology / Q000502:physiology*; D014407:Tumor Cells, Cultured / Q000187:drug effects / Q000276:immunology
D008222:Lymphokines