PT  - JOURNAL ARTICLE
AU  - Rasmussen, R
AU  - Takatsu, K
AU  - Harada, N
AU  - Takahashi, T
AU  - Bottomly, K
TI  - T cell-dependent hapten-specific and polyclonal B cell responses require release of interleukin 5.
DP  - 1988 Feb 01
TA  - The Journal of Immunology
PG  - 705--712
VI  - 140
IP  - 3
4099  - http://www.jimmunol.org/content/140/3/705.short
4100  - http://www.jimmunol.org/content/140/3/705.full
SO  - J. Immunol.1988 Feb 01; 140
AB  - CD4+ T cells in the mouse have recently been subdivided into two major subpopulations which differ in their functional activities and in the lymphokines they produce. Although cloned T cells lines representative of both sets will activate B cells in polyclonal responses, only the subset producing interleukin 4 (IL-4) will activate antigen-specific B cells in linked recognition assays. This suggested that IL-4 was essential for such responses. In the present experiments, the requirements were compared for B cell activation in specific as opposed to polyclonal antibody responses by T cell clones of the helper (IL-4 producing) subset. It was found that specific responses involve primarily small B cells, whereas polyclonal responses activate exclusively the large B cells. Second, polyclonal B cell responses can proceed in the absence of T:B contact, whereas specific responses require physical interaction of the two cells. Third, it was found that interleukin 5 (IL-5, formerly known as T cell replacing factor/B cell growth factor II) is essential for these polyclonal responses by inhibition of such responses with monoclonal anti-IL-5 antibody. Anti-IL-5 also inhibits specific antibody responses involving direct T:B interaction. Thus, IL-5 is clearly a critical mediator of differentiation to immunoglobulin secretion of activated B cells, whether such B cells are obtained as large B cells from freshly isolated spleen cells or are initially activated in an IL-4-dependent fashion by cognate interaction by a helper T cell clone.