Augmented humoral and anaphylactic responses in FcγRII-deficient mice

Toshiyuki Takai, Masao Ono, Masaki Hikida, Hitoshi Ohmori, Jeffrey V. Ravetch

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303 Citations (Scopus)


Despite its widespread distribution on both lymphoid and myeloid cells, the biological role of the low-affinity immunoglobulin-G receptor, FcγRII, is not fully understood. Defects in this receptor or its signalling pathway in B cells result in perturbations in immune-complex-mediated feedback inhibition of antibody production. We now report that FcγRII-deficient animals display elevated immunoglobulin levels in response to both thymus-dependent and thymus-independent antigens. Additionally, the effector arm of the allergic response is perturbed in these mice. Mast cells from FcγRII(-/-) are highly sensitive to IgG-triggered degranulation, in contrast to their wild-type counterparts. FcγRII-deficient mice demonstrate an enhanced passive cutaneous analphylaxis reaction, the result of a decreased threshold for mast-cell activation by FcγRIII crosslinking. These results demonstrate that FcγRII acts as a general negative regulator of immune-complex-triggered activation in vivo for both the afferent and efferent limbs of the immune response. Exploiting this property offers new therapeutic opportunities for the treatment of allergic and autoimmune disorders.

Original languageEnglish
Pages (from-to)346-349
Number of pages4
Issue number6563
Publication statusPublished - 1996 Jan 25
Externally publishedYes

ASJC Scopus subject areas

  • General


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