A possible role for the ␥ subunit of immunoglobulin Fc receptors (FcR) in mucosal defenses against intestinal nematode parasites was studied using age-matched FcR␥-knockout (FcR␥ ؊/؊ ) and wild-type (FcR␥ ؉/؉ ) C57BL/6 mice. Mice were infected subcutaneously with 3,000 infective larvae of Strongyloides venezuelensis, and the degree of infection was monitored by daily fecal egg counts and adult worm recovery on days 8 and 13 postinfection. Mucosal mast cell (MMC) responses were assayed by in situ intestinal mast cell counts in stained histological sections of the jejunum and by measuring mouse mast cell protease 1 (MMCP-1) release in serum using sandwich enzyme-linked immunosorbent assay. FcR␥ ؊/؊ mice had significantly higher egg counts (P < 0.01) and numbers of adult worms (P < 0.05) than FcR␥ ؉/؉ mice, but mastocytosis and serum MMCP-1 release were comparable. It was concluded that MMCP-1 release may be spontaneous, does not depend on mast cell degranulation via the FcR␥ signaling system, and appears to play no role in the expulsion of S. venezuelensis. The delay in worm expulsion in the FcR␥ ؊/؊ mice might be related to inability of the MMC to degranulate and release effector molecules other than MMCP-1, since FcR␥ deletion abrogates mast cell degranulative responses.Fc receptors (FcR) are hetero-oligomeric complexes present on most effector cells of the immune system and, upon crosslinking by their ligand (antigen-antibody complex), mediate phagocytosis, antibody-dependent cell-mediated cytotoxicity, activation of inflammatory cells, and many other effector responses (20). However, several of the FcR require for cell surface assemblage and signal transduction into the interior of the cell an additional chain, the homodimeric ␥ subunit (20). Targeted disruption of this subunit results in pleiotropic defects in cell functions, including the loss of immunoglobulin E (IgE)-mediated mast cell degranulation (27). This is because the high-affinity FcR for IgE (FcεRI), which is also associated with host resistance to parasitic infections (12), requires the ␥ subunit to express receptor-mediated cellular functions (20). Intestinal mucosal mastocytosis is observed in certain helminth infections, and it was therefore speculated that mast cells were important in the expulsion of Strongyloides ratti in rodents (19). Subsequently, in a series of experiments in infected rodents, it was demonstrated that mucosal mast cells (MMC) induced by the mast cell growth/differentiation factor interleukin 3 (IL-3) were the effector cells in the immune expulsion of Strongyloides spp. (1,3,8,17,18). The exact mechanism of the mast cellmediated parasite expulsion is still not clear, although it has been suggested that granular contents released by activated mast cells may be the ultimate effector molecules (7, 17). Since Fc ␥ subunit deletion results in loss of mast cell function, including degranulation and granular content release (27), the aim of this study was to determine whether the MMC-mediated parasite expulsion mechanism actuall...
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