Since B-1 cells were first described, their origin and function remain controversial. Given the ability to produce natural antibodies and large amounts of IL-10, there is a consensus about their role in innate immunity. More recently, however, B-1 cells have been associated to adaptive immunity as well, due to the demonstration of immunological memory and antigen presentation capability. Here we demonstrate that adoptive transfer of pre-sensitized B-1b cells (obtained from OVA-sensitized mice) to naïve B-1 deficient animals, drastically affects the ability of transplanted animals to mount an adaptive response upon immunization with OVA. In contrast to naïve B-1 populated mice, mice transplanted with sensitized B-1 exhibit lower anti-OVA antibody levels, milder footpad swelling in response to OVA subcutaneous injection and reduced granulomatous reaction to OVA-coated beads. Moreover, we show that these pre-sensitized B-1 cells, when acting as APCs, induce poor T cell proliferation in vitro when compared with macrophages or B-1 cells obtained from naïve mice. This property may be due in part to insufficient expression of the co-stimulatory molecule CD86, necessary for optimal antigen presentation. In conclusion, our data suggest a novel role for B-1 cells as part of suppressor mechanisms in the immune system.