| First Author | Takai T | Year | 1996 |
| Journal | Nature | Volume | 379 |
| Issue | 6563 | Pages | 346-9 |
| PubMed ID | 8552190 | Mgi Jnum | J:31133 |
| Mgi Id | MGI:78617 | Doi | 10.1038/379346a0 |
| Citation | Takai T, et al. (1996) Augmented humoral and anaphylactic responses in Fc gamma RII-deficient mice. Nature 379(6563):346-9 |
| abstractText | Despite its widespread distribution on both lymphoid and myeloid cells, the biological role of the low-affinity immunoglobulin-G receptor, Fc gamma RII, 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 Fc gamma RII-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 Fc gamma RII-/- are highly sensitive to IgG-triggered degranulation, in contrast to their wild-type counterparts. Fc gamma RII-deficient mice demonstrate an enhanced passive cutaneous analphylaxis reaction, the result of a decreased threshold for mast-cell activation by Fc gamma RIII cross-linking. These results demonstrate that Fc gamma RII 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. |
