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Lymphocyte Biology Section, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892
T cell activation requires exposure to processed Ag and signaling
by cytokines and costimulatory ligands. Adjuvants are thought to
enhance immunity primarily through up-regulation of the latter signals.
Here, we explore the effect of the bacterial adjuvant, endotoxin, on Ag
presentation by B cells and dendritic cells (DC). Using an mAb (C4H3)
specific for the hen egg lysozyme (HEL) 46-61 determinant bound to
I-Ak, we analyze processed Ag expression and the tissue
distribution of presenting cells following systemic administration of
soluble HEL to mice. In both LPS-responsive and -hyporesponsive mice
given endotoxin-containing HEL, B cells rapidly display surface
46-61/I-Ak complexes. In marked contrast, in
LPS-hyporesponsive mice, splenic DC show little gain in C4H3 staining.
In LPS-responsive animals, interdigitating DC in T cell areas show no
staining above background at early times after HEL administration, but
C4H3+ DC rapidly accumulate in the outer periarteriolar
lymphoid sheaths (PALS) and in follicular areas. Within a few hours,
C4H3+ DC appear in the T cell areas, concomitant with a
decline in C4H3+ cells in the outer PALS, suggesting
migration between these two sites. Endotoxin enhancement of C4H3
staining is seen for both CD8
- and CD8+
DC subsets. These data suggest that a major effect of adjuvants is to
promote mobilization of Ag-bearing DC to the T areas of lymphoid
tissue, and possibly also to enhance Ag processing by these DC. Thus,
microbial products promote T cell immunity not only through DC
activation for cosignaling, but through improvement in signal 1
delivery.
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