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*
Division of Immunology, University of Cincinnati College of Medicine, Cincinnati, OH 45267;
Cincinnati Veterans Affairs Medical Center, Cincinnati, OH 45220;
Department of Microbiology, University of Alabama, Birmingham, AL 35294; and
§
Division of Pediatric Rheumatology, Children’s Hospital Medical Center, Cincinnati, OH 45229
We report that IL-4 causes a redistribution of B cells and modestly
increases B cell life span. Intravenous injection of a long-acting
formulation of IL-4 induces increases in both spleen cell number and
the percentage of splenic B cells. These effects are observed within 1
day of IL-4 administration and plateau after 
3 days if IL-4
treatment is continued. The increase in splenic B cell number is IL-4
dose dependent, CD4+ T cell independent, Fc
RII/FcRIII
independent, and Stat6 independent. Decreases in the number of B cells
in the blood and the percentage of mature B cells in the bone marrow,
concomitant with the increase in splenic B cell number, suggest that
redistribution of circulating B cells to the spleen is partially
responsible for IL-4 induction of splenic B cell hyperplasia.
Considerable reduction in the effect of 5 days of IL-4 treatment on
splenic B cell number when B lymphopoiesis is blocked with
anti-IL-7 mAb suggests that generation of new B cells is also
involved in IL-4-induced splenic B cell hyperplasia.
5-Bromo-2'-deoxyuridine labeling experiments demonstrate that IL-4
modestly prolongs the life span of newly generated splenic B cells, and
experiments that measure B cell HSA (CD24) expression as an indicator
of B cell age suggest that IL-4 may also prolong the life span of
mature splenic B cells. Thus, IL-4 increases splenic B cell number
through two Stat6-independent effects: increased net migration of
circulating B cells to the spleen and increased B cell life span. Both
effects may promote Ab responses to a systemic Ag
challenge.
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