Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 194, Issue 2, Pages 227-233Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.194.2.227
Keywords
mast cells; immunoreceptor tyrosine-based inhibitory motif passive cutaneous anaphylaxis; active cutaneous anaphylaxis; active systemic anaphylaxis
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Funding
- NHLBI NIH HHS [HL36110] Funding Source: Medline
- NIAID NIH HHS [AI40171, AI07306, AI41144, AI31599, AI22531] Funding Source: Medline
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gp49B1 is an immunoglobulin (Ig) superfamily member that inhibits Fc is an element of RI-induced mast cell activation when the two receptors are coligated with antibodies in vitro. The critical question of in vivo function of gp49B1 is now addressed in gene-disrupted mice. gp49B1-deficient mice exhibited a significantly increased sensitivity to IgE-dependent passive cutaneous anaphylaxis as assessed by greater tissue swelling and mast cell degranulation in situ. Importantly, by the same criteria, the absence of gp49B1 also resulted in a lower threshold for antigen challenge in active cutaneous anaphylaxis, in which the antigen-specific antibody levels were comparable in gp49B1-deficient and sufficient mice. Moreover, the absence of gp49B1 resulted in a significantly: greater and faster death rate in active systemic anaphylaxis. These results indicate that gp49B1 innately dampens adaptive immediate hypersensitivity responses by suppressing mast cell activation in vivo. In addition, this study provides a new concept and target for regulation of allergic disease susceptibility and severity.
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