IgE antibodies play a key role in the development of allergic reactions. Non-specific immunotherapy which enables to control the IgE dependent response at either the synthesis level or the effector phase can be an effective therapeutic agent for atopic diseases. To decrease the quantity of IgE anti-IgE molecules have been developed. Humanized monoclonal antibodies (mAbs) CGP 51901, CGP 56901 and rhuMAb E25 are currently under clinical studies. They bind to the C epsilon 3 domain of human free IgE and surface IgE of IgE expressing B cells but not to IgE bound to high affinity IgE receptors (Fc epsilon RI) on mast cells and basofils or low affinity IgE receptors (Fc epsilon RII) on other cells, and therefore they do not release the histamine and other mediators from these cells. Intravenous administration of anti-IgE mAb reduces circulating levels of IgE in atopic patients to low levels commonly seen in non-atopic individuals. Anti-IgE therapy offers protection against allergen-induced bronchoconstriction and reduces severity of symptoms of allergic rhinitis. Anti-IgE mAbs produce improvement in lung function and symptom control, they reduce the need for short acting inhaled beta 2-agonist and corticosteroids among asthmatic patients. Anti-IgE mAb are well tolerated. They do not induce anaphylaxis and the occurrence of antibodies against anti-IgE mAb is sporadic. The results of cited studies suggest that humanized anti-IgE monoclonal antibodies may have important immunotherapeutic benefit for treatment of allergic disorders.