*P< 005; **P< 001 To investigate the relative dominance of Th2 versus the Th1 immune response, we determined the mRNA expression of IL-4 in relation to IFN-. migration of B cells and natural killer cells to airways and reduced levels of allergen-specific IgG and IgA in bronchoalveolar lavage fluid. The role for B cells in the airway inflammation was indicated by the impaired ability of mice lacking functional B cells to evoke an eosinophilic response. The diminished eosinophilia in TCR KO mice could not be explained by a defective Th2 activation since these mice displayed a normal IgG response in serum and an unaffected IG2b/IgG1 ratio in airways. Analysis of immunoregulatory cytokines in isolated lung tissue, thoracic lymph nodes and spleen further supported the notion that these mice are able to evoke a sufficient activation of T helper cells and that T cells are not required for maintaining the Th2 profile. These results indicate that T cells contribute to allergic airway inflammation by pathways individual from classical Th2 immune activation. == Introduction == Lymphocytes expressing the T-cell receptor (TCR) comprise less than 10% of the T-cell populace in lymphoid organs and peripheral blood.1A specific localization of T cells in the epithelium has been postulated, based on the observations that these cells are increased among intraepithelial lymphocytes (IEL) in the gastrointestinal tract and by the skewed repertoire of TCR V and V genes expressed by human and mouse IEL.28Several studies have demonstrated that T cells expressing a similar V and V repertoire as in IEL are increased in the circulation of patients with inflammatory bowel disease and in the joints of patients with rheumatoid arthritis.2,918Similarly, it is reported that this subset of T cells is usually enriched in the airway epithelium of patients with allergic inflammation.19Although it is strongly suggested from these studies that T cells are involved in the progression or regulation of inflammatory disorders, it has not been possible to definitely define the role for T cells in human diseases. Experimentally induced inflammation in rodents may be helpful to unravel the role of T cells in various inflammatory disorders. Adjuvant-induced arthritis in rats is usually a T-cell dependent disease affecting peripheral joints.20,21Depletion of T cells before injection of the adjuvants, mineral MSK1 oil22squalene23or Freund’s complete adjuvant24does not affect the disease course measured as joint swelling, although microscopic aggravation of joint destruction has been observed in animals depleted of T cells.24Adjuvant-induced airway inflammation, provoked by inhalation of bacterial endotoxin (lipopolysaccharide; AKR1C3-IN-1 LPS), is usually similarly to adjuvant-induced arthritis controlled by CD4+T cells.25In this model of acute airway inflammation, we have recently demonstrated that mice lacking T cells and the corresponding wild-type strain do not differ in the accumulation of neutrophils in airspaces.26However, Penidoet al. reported that T cells are required for eosinophil migration into the lungs AKR1C3-IN-1 after inthrathoracic injection of LPS.27Thus, under certain experimental conditions T cells may contribute to the migration of granulocytes into the inflamed loci and it appears that eosinophils rather than neutrophils are controlled by this T-cell subset. In mouse models of allergic hyperresponsiveness induced by sensitization to an allergen followed by inhalation challenge, it has been recently shown that T cells AKR1C3-IN-1 participate in airway inflammation.2830This disease differs from adjuvant-induced inflammation by the dependency of a specific T helper 2 (Th2)-dominated T helper response against the immunized antigen and is characterized by accumulation of eosinophils rather than neutrophils in airspaces.31,32Whether T cells are involved in the type 2 response or promote the eosinophilia through some other mechanism is controversial. In a model of adoptive transfer of T.