title: Gammadelta T lymphocytes producing IFNgamma and IL-17 in response to Candida albicans or mycobacterial antigens: possible implications for acute and chronic inflammation.
abstract: T lymphocytes bearing the gammadelta T cell receptor are known to play an important role in the first-line defense against viral, bacterial and fungal pathogens. Two main subsets of gammadelta T cells are known, showing distinct functional behaviour: Vdelta2 T lymphocytes, circulating in the peripheral blood, are involved in the response to mycobacterial infections and certain viruses, including coxsakie virus B3 and herpes simplex virus type 2. Vdelta1 T cells are resident in the mucosal-associated lymphoid tissue and are reported to participate in the immunity against Listeria monocytogenes and cytomegalovirus. Vdelta2 T lymphocytes recognize non-peptidic phosphorylated metabolites of isoprenoid biosynthesis, expressed by mycobacteria, while Vdelta1 T cells mainly interact with MHC-related antigens (MIC-A and MIC-B) and with receptors, called UL-16 binding proteins, for the UL-16 protein produced by cytomegalovirus-infected cells. Both Vdelta1 and Vdelta2 T cells can produce interferon-gamma in response to MIC-A(+) cells or non-peptide antigens, respectively. Moreover, production of TNF-alpha by human Vgamma9/Vdelta2 T cells has been demonstrated in response to bacterial products and non-peptidic molecules. Recently, it has been reported that gammadelta T lymphocytes can produce IL-17 during Escherichia coli or Mycobacterium tuberculosis infections in mice. This is of interest as IL-17 is emerging as a cytokine crucial in the control of intracellular pathogens and fungi. In this review, we will discuss the possible role of IL-17 producing gammadelta T cells in the regulation of acute and chronic inflammation, focusing on the different response of the two subsets to mycobacterial, viral or fungal antigens.
authors.affiliation: Laboratory of Molecular Oncology and Angiogenesis, National Institute for Cancer Research, 16132-Genoa, Italy. alessandro.poggi@istge.it
authors.forename: A
authors.initials: A
authors.lastname: Poggi
authors.forename: S
authors.initials: S
authors.lastname: Catellani
authors.forename: A
authors.initials: A
authors.lastname: Musso
authors.forename: M R
authors.initials: MR
authors.lastname: Zocchi
mesh_terms: D000208:Acute Disease; D000818:Animals; D000942:Antigens, Bacterial / Q000276:immunology*; D002176:Candida albicans / Q000276:immunology*; D002454:Cell Differentiation; D002908:Chronic Disease; D006801:Humans; D007249:Inflammation / Q000276:immunology*; D007371:Interferon-gamma / Q000378:metabolism*; D020381:Interleukin-17 / Q000378:metabolism*; D051379:Mice; D009169:Mycobacterium tuberculosis / Q000276:immunology*; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000032:analysis*; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: D000942:Antigens, Bacterial; D020381:Interleukin-17; D016692:Receptors, Antigen, T-Cell, gamma-delta; D007371:Interferon-gamma