TY - JOUR
T1 - From normal to clonal B cells
T2 - Chronic lymphocytic leukemia (CLL) at the crossroad between neoplasia and autoimmunity
AU - Ghia, Paolo
AU - Scielzo, Cristina
AU - Frenquelli, Michela
AU - Muzio, Marta
AU - Caligaris-Cappio, Federico
PY - 2007/12
Y1 - 2007/12
N2 - Chronic lymphocytic leukemia (CLL) is a B-cell malignancy endowed with a number of features that recall autoimmune disorders, including the CD5 expression and the development of autoimmune manifestations restricted to self antigens expressed by hematopoietic cells. Several evidences strongly support the possibility that an antigenic stimulation through the B-cell receptor (BCR) is involved in the selection and possibly also the expansion of the malignant clone. Though all evidences suggest specific Ag recognition and possibly stimulation at different time-points, the nature of the Ag(s) is still unknown. It appears likely that CLL cells derive from a pool of auto/polyreactive CD5+ B cells. Hence CLL appears to be a B-cell malignancy triggered or facilitated in its development and evolution by an auto-Ag. The crucial issues have become to what extent this deleterious binding capacity is central to the natural history of the disease and how it relates to the malignant transformation of the cell.
AB - Chronic lymphocytic leukemia (CLL) is a B-cell malignancy endowed with a number of features that recall autoimmune disorders, including the CD5 expression and the development of autoimmune manifestations restricted to self antigens expressed by hematopoietic cells. Several evidences strongly support the possibility that an antigenic stimulation through the B-cell receptor (BCR) is involved in the selection and possibly also the expansion of the malignant clone. Though all evidences suggest specific Ag recognition and possibly stimulation at different time-points, the nature of the Ag(s) is still unknown. It appears likely that CLL cells derive from a pool of auto/polyreactive CD5+ B cells. Hence CLL appears to be a B-cell malignancy triggered or facilitated in its development and evolution by an auto-Ag. The crucial issues have become to what extent this deleterious binding capacity is central to the natural history of the disease and how it relates to the malignant transformation of the cell.
KW - Auto-antigen
KW - B lymphocytes
KW - CD5
KW - Chronic lymphocytic leucemia
KW - Immunoglobulin receptor
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U2 - 10.1016/j.autrev.2007.02.014
DO - 10.1016/j.autrev.2007.02.014
M3 - Article
C2 - 18035322
AN - SCOPUS:34948854157
VL - 7
SP - 127
EP - 131
JO - Autoimmunity Reviews
JF - Autoimmunity Reviews
SN - 1568-9972
IS - 2
ER -