title: Immunologic abnormalities exhibited in IL-7 transgenic mice with dermatitis.
abstract: Interleukin (IL)-7 transgenic mice, which we established previously, developed severe dermatitis characterized by massive infiltration of gammadelta T cells in the dermal lesion. To fully understand the pathology of this intriguing skin disease, we examined several immunologic features of dermis infiltrating lymphocytes from the lesional skin of IL-7 transgenic mice. We observed a moderate response to mitogens, a poor response to alloantigens, and the absence of cytotoxic activities to several tumor cell lines and skin derived cells regardless of the presence of IL-2 or IL-7. On the other hand, dermis infiltrating lymphocytes could proliferate with exogenous IL-2 and IL-7. Moreover, reverse transcriptase polymerase chain reaction and fluorescence activated cell sorter analysis revealed that dermis infiltrating lymphocytes expressed various cytokines including IL-4 and IL-7, and several activation markers for T cells (CD44, CD69, IL-2R alpha), in addition to IL-7R alpha. In the sera of the affected mice, hyper epsilon-globulinemia was observed. These findings suggested that dermis infiltrating lymphocytes proliferated in an activated state in the skin lesion in an autocrine and/or paracrine manner and produced Th2 type cytokines that might evoke immunologic abnormalities. This study and previous findings suggest that IL-7 transgenic mouse with dermatitis offer the potential of serving as a useful tool for investigating the immunologic role of cutaneous gammadelta T cells, especially their participation in IgE production in vivo.
authors.affiliation: Shionogi Institute for Medical Science, Osaka, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Uehira
authors.forename: H
authors.initials: H
authors.lastname: Matsuda
authors.forename: A
authors.initials: A
authors.lastname: Nakamura
authors.forename: H
authors.initials: H
authors.lastname: Nishimoto
mesh_terms: D000818:Animals; D015415:Biomarkers; D002455:Cell Division / Q000187:drug effects / Q000502:physiology; D002462:Cell Membrane / Q000378:metabolism; D002465:Cell Movement / Q000187:drug effects / Q000502:physiology; D002470:Cell Survival / Q000502:physiology; D016207:Cytokines / Q000235:genetics / Q000494:pharmacology; D003872:Dermatitis / Q000097:blood / Q000235:genetics* / Q000276:immunology*; D007073:Immunoglobulin E / Q000032:analysis; D015851:Interleukin-7 / Q000235:genetics*; D008214:Lymphocytes / Q000187:drug effects / Q000473:pathology / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic / Q000235:genetics*; D008934:Mitogens / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D012867:Skin / Q000276:immunology; D013154:Spleen / Q000166:cytology / Q000502:physiology; D018417:Th1 Cells / Q000378:metabolism; D018418:Th2 Cells / Q000378:metabolism; D014407:Tumor Cells, Cultured
chemical_list: D015415:Biomarkers; D016207:Cytokines; D015851:Interleukin-7; D008934:Mitogens; D012333:RNA, Messenger; D007073:Immunoglobulin E