Paradoxically, despite the presence of high systemic TNF levels during infection [38] and the clear evidence shown here that transitional B cell loss through apoptosis coincides with elevation of Fas expression on both T1 and T2 B cells, our results showed through the use of knock-out mice as well as anti-FasL antibodies that neither the TNF- nor the Fas- death pathways acting alone are responsible for transitional B cell apoptosis in a T. brucei infection setting. Here, TNF is linked to infection.