Abstract

Mice with malaria showed unique immunological responses, including the expansion of NK1.1 −TCR int cells (extrathymic T cells). Since TCR int cells with autoreactivity and autoantibody-producing B cells (B-1 cells) are often simultaneously activated under autoimmune conditions, it was examined whether B-1 cells were activated in the course of malarial infection. From days 14 after infection, B220 low B-1 cells appeared in the liver and spleen. The number of B220 low B cells was highest at day 14, but the ratio was highest at days 28–35. In parallel with the appearance of B220 low cells, autoantibodies against HEp-2 cells and double-stranded DNA were detected in sera. These B220 low cells had phenotypes of CD44 high, CD23 − and CD62L −. In sharp contrast, conventional B220 high B cells (B-2 cells) were CD44 low, CD23 + and CD62L +. These results suggested that malaria immune responses were not mediated by conventional T and B cells but resembled the responses during autoimmune diseases.

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