The ability of Th cells, type 1 (T[H1]), to activate and induce differentiation of B cells into antibody-secreting cells is controversial because 1) some clones of T(H1) cells provide help while others do not, and 2) by using the same T(H1) clone, different laboratories disagree on whether they provide help to B cells. One possible explanation for the latter is the variability in the activation status of the B cells used in different laboratories. In the present studies, we have used Ag-specific B cells from athymic (nu/nu) mice, or sterilely housed nu/+ mice to study the T(H1)-mediated activation of B cells that had received little or no prior help from T cells and/or antigen in vivo. These B cells express low levels of surface Ia (sIa) Ag, and fail to secrete IgG2a in response to T(H1) cells plus Ag; in contrast, responses to T(H2) cells plus Ag are normal. To explore this observation further, we prepared 'surface(s) Ia(lo)' B cells from conventionally housed BALB/c mice by sorting spleen cells on the fluorescence-activated cell sorter. This sIa(lo) population also failed to produce IgG2a in response to T(H1) cells plus Ag. In contrast, the SIa(Hi), (presumably more mature) B cells, responded to both the T(H1) and T(H2) cells. The addition of LPS, T(H2) cells or the lymphokine, IL-4, to cultures of sIa(lo) B cells from normal or nu/nu mice (plus Ag and T(H1) cells), restored IgG2a responses to control levels. Low sIa levels were not the sole cause of nonresponsiveness of the nu/nu B cells because a 24-h pulse with IL-4 restored sIa to control levels without restoring IgG2a production after activation with T(H1) cells plus Ag. These data support the conclusion that sIa(lo) B cells are immature and require an activation/maturation signal from IL-4 in vivo in order to respond to T(H1) cells and Ag in vitro.
|Original language||English (US)|
|Number of pages||6|
|Journal||Journal of Immunology|
|State||Published - 1990|
ASJC Scopus subject areas
- Immunology and Allergy