Secondary intratracheal infection of mice with Mycoplasma pulmonis generates IgG1 memory B cells

Mycoplasma pulmonis, a rodent respiratory pathogen, was used to study the immune response in the bronchus-associated lymphoid tissue (BALT) and other lymphoid tissues. Infection of BALB/c mice intratracheally (i.t.) with M. pulmonis results in an increased frequency of antigen-sensitive B cells at the site of priming. Upon secondary i.t. challenge, the frequency of antigen-specific B cells rises significantly in BALT, in peripheral blood and, to a lesser extent, in lymphoid tissues distal to the site of priming, i.e., spleen and Peyer's patches. The predominant isotype of anti-M. pulmonis antibody expressed by clones grown in thymus-dependent splenic fragment cultures from B cells taken from all tissues is IgG1. Elimination of accompanying T cells in inocula from euthymic BALB/c mice or lack of T cells at the time of in vivo priming of athymic mice does not change the isotype profile of clones grown from M. pulmonis-specific B cells. The splenic fragment cultures used to grow these clones do not distort the isotype display towards IgG1 expression, since clones grown from either primed or unprimed B cells of other specificities (i.e., trinitrophenyl--TNP) express any or all isotypes in a variety of combinations. The majority of M. pulmonis-specific clonal precursor B cells are sIgG1+/IgD-. All these findings suggest that the potential to give rise to predominantly IgG1-secreting clones in vitro is intrinsic to the M. pulmonis-specific memory B cells primed in vivo.