B cell from aged mice exhibit reduced apoptosis upon BCR stimulation and differential ability to up-regulate survival signals.

MONTES C; MALETTO B; ACOSTA RODRIGUEZ E; GRUPPI A; PISTORESI-PALENCIA MC

CLINICAL AND EXPERIMENTAL IMMUNOLOGY

Blackwell Science

Año: 2006 vol. 143 p. 30 - 40

0009-9104

During ageing, autoimmune disorders and the higher susceptibility to infectious have been associated with alterations in the humoral immune response. We report that splenic B lymphocytes from aged mice exhibit lower level of apoptosis induced by B-cell antigen receptor (BCR) ligation in vitro . Respect to B cells from young mice the anti-ìì stimulated aged B cells show similar Bcl- 2 and Bcl-xL expression but differential kinetic of A1 degradation and a higher level of cFLIP and FAIM. Even though B cells from aged mice show minor Fas expression they exhibit the same susceptibility to anti-Fas induced apoptosis. Aged B cells also present upon BCR stimulation, a higher proliferative response and similar level of activation markers expression than B cells from young mice. These data agree with the observation that aged mice exhibit an increment of T2 and mature B cell subset which rapidly enters cell cycle upon BCR engagement. The diminished apoptosis after activation in aged mice could compromise homeostatic mechanism allowing the persistence of self and non-self antigen specific B cells.