TY - JOUR
T1 - β2-Microglobulin-dependent NK1.1+ T cells are not essential for T helper cell 2 immune responses
AU - Brown, Daniel R.
AU - Fowell, Deborah J.
AU - Corry, David B.
AU - Wynn, Thomas A.
AU - Moskowitz, Naomi H.
AU - Cheever, Allen W.
AU - Locksley, Richard M.
AU - Reiner, Steven L.
PY - 1996/10/1
Y1 - 1996/10/1
N2 - A number of investigation have established the critical role of interleukin 4 (IL-4) in mediating the development of T helper (Th)2 effector cells in vitro and in vivo. Despite intensive study, the origin of the IL-4 required for Th2 priming and differentiation remains unclear. Natural killer (NK)1.1+ α/β T cell receptor+ T (NT) cells, a unique lineage of cells capable of producing large amounts of IL-4 after activation in vivo, are important candidates for directing Th2 priming. These cells are selected by the nonpolymorphic major histocompatibility complex (MHC) class I molecule, CD1, and are deficient in β2-microglobulin (β2m)-null mice. We used Th2 immune responses after challenge with a number of well-characterized antigens administered by a variety of routes. As assessed by immunization with protein antigen, infection with Leishmania major, embolization with eggs of Schistosoma mansoni, intestinal infection with Nippostrongylus brasiliensis, or induction of airway hyperactivity to aerosolized antigen, β2m-deficient mice developed functional type 2 immune responses that were not substantially different than those in wild-type mice. Production of IL-4 and the generation of immunoglobulin E (IgE) and eosinophil responses were preserved as assessed by a variety of assays. Collectively, these results present a comprehensive analysis of type 2 immune responses in β2m-deficient mice, and indicate that β2m-dependent NT cells are not required for Th2 development in vivo.
AB - A number of investigation have established the critical role of interleukin 4 (IL-4) in mediating the development of T helper (Th)2 effector cells in vitro and in vivo. Despite intensive study, the origin of the IL-4 required for Th2 priming and differentiation remains unclear. Natural killer (NK)1.1+ α/β T cell receptor+ T (NT) cells, a unique lineage of cells capable of producing large amounts of IL-4 after activation in vivo, are important candidates for directing Th2 priming. These cells are selected by the nonpolymorphic major histocompatibility complex (MHC) class I molecule, CD1, and are deficient in β2-microglobulin (β2m)-null mice. We used Th2 immune responses after challenge with a number of well-characterized antigens administered by a variety of routes. As assessed by immunization with protein antigen, infection with Leishmania major, embolization with eggs of Schistosoma mansoni, intestinal infection with Nippostrongylus brasiliensis, or induction of airway hyperactivity to aerosolized antigen, β2m-deficient mice developed functional type 2 immune responses that were not substantially different than those in wild-type mice. Production of IL-4 and the generation of immunoglobulin E (IgE) and eosinophil responses were preserved as assessed by a variety of assays. Collectively, these results present a comprehensive analysis of type 2 immune responses in β2m-deficient mice, and indicate that β2m-dependent NT cells are not required for Th2 development in vivo.
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U2 - 10.1084/jem.184.4.1295
DO - 10.1084/jem.184.4.1295
M3 - Article
C2 - 8879201
AN - SCOPUS:0029959243
VL - 184
SP - 1295
EP - 1304
JO - Journal of Experimental Medicine
JF - Journal of Experimental Medicine
SN - 0022-1007
IS - 4
ER -