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γδ T cells contribute to the systemic immunoglobulin E response and local B‐cell reactivity in allergic eosinophilic airway inflammation
Author(s) -
Svensson Linda,
Lilliehöök Bo,
Larsson Roland,
Bucht Anders
Publication year - 2003
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.2003.01561.x
Subject(s) - immunology , immunoglobulin e , eosinophilia , ovalbumin , t cell , cytotoxic t cell , antibody , biology , immune system , medicine , in vitro , biochemistry
Summary Allergic airway inflammation induced in mice is T‐cell dependent and recruitment of eosinophils to airspaces requires both αβ and γδ T cells. From previous studies it is evident that αβ T cells are essential for the allergic T helper type 2 (Th2)‐like response, while the mechanistic contribution of γδ T cells is still unclear. In this study, we have investigated the role of γδ T cells in allergic airway eosinophilia induced by ovalbumin hypersensitivity. By comparing the responsiveness to sensitizing allergen of wild‐type mice with that of T‐cell receptor γδ knockout mice (TCRγδ KO) we demonstrated that mice lacking γδ T cells are defective in the systemic ovalbumin‐specific immunoglobulin E (IgE) response. Furthermore, after aerosol challenge with allergen, γδ T‐cell deficient mice exhibited a significantly decreased 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 TCRγδ KO mice could not be explained by a defective Th2 activation since these mice displayed a normal IgG response in serum and an unaffected IG2 b /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 γδ T cells are not required for maintaining the Th2 profile. These results indicate that γδ T cells contribute to allergic airway inflammation by pathways separate from classical Th2 immune activation.