title: IL-13 from Th2-type cells suppresses induction of antigen-specific Th1 immunity in a T-cell lymphoma.
abstract: Dalton's lymphoma (DL) is a transplantable T-cell lymphoma of spontaneous origin, characterized by highly invasive and immunosuppressive property. Progression of DL cells results into an imbalance of T helper type 1 (T(h)1)/T helper type 2 (T(h)2)-type cytokine in the host, which is partly responsible for DL-induced severe immunosuppression and DL cell progression. In this study, we have shown the role of IL-13 in the regulation of T(h)1 immunity in both normal healthy and DL-bearing host. IL-13 pre-treatment inhibits the induction of 2,4-dinitro-1-fluorobenzene-induced contact hypersensitivity and delayed-type hypersensitivity (DTH) in antigen-challenged mice, which have been confirmed by neutralizing IL-13 by systemic delivery of non-signaling decoy receptor IL-13Ralpha2. Furthermore, IL-13 neutralization enhances the splenocyte proliferation, which has been inhibited by IL-13 administration. Adoptive transfer of splenocyte from IL-13-pre-treated mice and macrophages incubated with IL-13 and pulsed with antigens suppresses the DTH as well in antigen-challenged recipient mice. In addition, it also suppresses the production of pro-inflammatory cytokine and C-C chemokine in DTH footpad. Furthermore, IL-13 neutralization not only enhances the DTH reaction but also increases longevity and survival of DL-bearing host, which suggests that blocking/inactivating systemic IL-13 enhances T(h)1 immunity, and therefore, effects to diminish IL-13 production may have therapeutic value in a host bearing T-cell lymphoma.
authors: Centre of Advanced Study in Zoology, Department of Zoology, Faculty of Science, Banaras Hindu University, Varanasi 221 005, Uttar Pradesh, India.
authors: Praveen
authors: P
authors: Deepak
authors: Sanjay
authors: S
authors: Kumar
authors: Dhiraj
authors: D
authors: Kishore
authors: Arbind
authors: A
authors: Acharya
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D000951:Antigens, Neoplasm / Q000276:immunology; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D054405:Chemokine CCL3 / Q000378:metabolism; D003877:Dermatitis, Contact / Q000276:immunology* / Q000473:pathology; D004139:Dinitrofluorobenzene / Q000008:administration & dosage / Q000031:analogs & derivatives; D006968:Hypersensitivity, Delayed / Q000276:immunology* / Q000473:pathology; D007371:Interferon-gamma / Q000378:metabolism; D018793:Interleukin-13 / Q000276:immunology* / Q000494:pharmacology; D053663:Interleukin-13 Receptor alpha2 Subunit / Q000276:immunology; D008213:Lymphocyte Activation / Q000187:drug effects; D016399:Lymphoma, T-Cell / Q000276:immunology* / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D009368:Neoplasm Transplantation; D018417:Th1 Cells / Q000187:drug effects / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D018418:Th2 Cells / Q000187:drug effects / Q000276:immunology / Q000378:metabolism* / Q000473:pathology
chemical_list: D000951:Antigens, Neoplasm; D054405:Chemokine CCL3; D018793:Interleukin-13; D053663:Interleukin-13 Receptor alpha2 Subunit; D007371:Interferon-gamma; D004139:Dinitrofluorobenzene; C002041:1,5-difluoro-2,4-dinitrobenzene