In the field of allergic diseases, extensive research has demonstrated the implication of a strong TH2 activation that both initiates and maintains in situ inflammation with the help of TH2 cytokines. However, as anti-TH2 cytokines therapy is not sufficient to suppress the disease, a more complex immunological mechanism is suspected. In this review, we will revisit the TH2 dogma in allergic diseases, propose a possible implication of TH1 inflammation correlated with the severity of atopic disease, to conclude with the therapeutic solutions envisaged.