title: CD30 is required for activation of a unique subset of interleukin-17A-producing γδ T cells in innate immunity against Mycobacterium bovis Bacillus Calmette-Guerin infection.
abstract: Interleukin-17A (IL-17A)-producing γδ T cells are known to be activated following Mycobacterium bovis bacillus Calmette-Guérin (BCG) infection. Here, we show that CD30, a member of the tumor necrosis factor (TNF) receptor superfamily, is important for activation of IL-17A-producing γδ T cells after BCG infection. Vγ1(-) Vγ4(-) γδ T cells preferentially expressing Vγ6/Vδ1 genes were identified as the major source of IL-17A in the peritoneal cavity during the early stage of BCG infection. The number of IL-17A-producing Vγ1(-) Vγ4(-) γδ T cells bearing Vγ6 increased in peritoneal exudate cells (PEC) of wild-type (WT) mice but not in those of CD30 knockout (KO) mice in response to BCG infection. Consistently, CD30 ligand (CD30L) or CD30 expression, predominantly by Vγ1(-) Vγ4(-) γδ T cells, was rapidly upregulated after BCG infection. Inhibition of CD30L/CD30 signaling by in vivo administration of a soluble CD30 and immunoglobulin fusion protein (CD30-Ig) severely impaired activation of IL-17A-producing Vγ1(-) Vγ4(-) γδ T cells in WT mice, while stimulating CD30L/CD30 signaling by in vivo administration of agonistic anti-CD30 monoclonal antibody (MAb) restored IL-17A production by Vγ1(-) Vγ4(-) γδ T cells in CD30L KO mice after BCG infection. These results suggest that CD30 signaling plays an important role in the activation of IL-17A-producing Vγ1(-) Vγ4(-) γδ T cells bearing Vγ6 at an early stage of BCG infection.
authors.affiliation: Division of Host Defense, Medical Institute of Bioregulation.
authors.forename: Ying
authors.initials: Y
authors.lastname: Guo
authors.forename: Xun
authors.initials: X
authors.lastname: Sun
authors.forename: Kensuke
authors.initials: K
authors.lastname: Shibata
authors.forename: Hisakata
authors.initials: H
authors.lastname: Yamada
authors.forename: Hiromi
authors.initials: H
authors.lastname: Muta
authors.forename: Eckhard R
authors.initials: ER
authors.lastname: Podack
authors.forename: Yasunobu
authors.initials: Y
authors.lastname: Yoshikai
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal; D001202:Ascitic Fluid / Q000166:cytology; D053285:CD30 Ligand / Q000235:genetics / Q000378:metabolism; D016207:Cytokines; D005786:Gene Expression Regulation / Q000276:immunology; D007113:Immunity, Innate / Q000502:physiology*; D020381:Interleukin-17 / Q000235:genetics / Q000378:metabolism*; D017730:Ki-1 Antigen / Q000235:genetics / Q000378:metabolism*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009163:Mycobacterium bovis; D016176:T-Lymphocyte Subsets / Q000378:metabolism*; D014376:Tuberculosis / Q000276:immunology* / Q000382:microbiology
chemical_list: D000911:Antibodies, Monoclonal; D053285:CD30 Ligand; D016207:Cytokines; D020381:Interleukin-17; D017730:Ki-1 Antigen; C505775:Tnfsf8 protein, mouse
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