title: Reduced immune response to Borrelia burgdorferi in the absence of γδ T cells.
abstract: Little is known regarding the function of γδ T cells, although they accumulate at sites of inflammation in infections and autoimmune disorders. We previously observed that γδ T cells in vitro are activated by Borrelia burgdorferi in a TLR2-dependent manner. We now observe that the activated γδ T cells can in turn stimulate dendritic cells in vitro to produce cytokines and chemokines that are important for the adaptive immune response. This suggested that in vivo γδ T cells may assist in activating the adaptive immune response. We examined this possibility in vivo and observed that γδ T cells are activated and expand in number during Borrelia infection, and this was reduced in the absence of TLR2. Furthermore, in the absence of γδ T cells, there was a significantly blunted response of adaptive immunity, as reflected in reduced expansion of T and B cells and reduced serum levels of anti-Borrelia antibodies, cytokines, and chemokines. This paralleled a greater Borrelia burden in γδ-deficient mice as well as more cardiac inflammation. These findings are consistent with a model of γδ T cells functioning to promote the adaptive immune response during infection.
authors.affiliation: Vermont Center for Immunology and Infectious Diseases, The University of Vermont College of Medicine, Burlington, VT 05405-0068, USA.
authors.forename: Cuixia
authors.initials: C
authors.lastname: Shi
authors.forename: Bikash
authors.initials: B
authors.lastname: Sahay
authors.forename: Jennifer Q
authors.initials: JQ
authors.lastname: Russell
authors.forename: Karen A
authors.initials: KA
authors.lastname: Fortner
authors.forename: Nicholas
authors.initials: N
authors.lastname: Hardin
authors.forename: Timothy J
authors.initials: TJ
authors.lastname: Sellati
authors.forename: Ralph C
authors.initials: RC
authors.lastname: Budd
mesh_terms: D056704:Adaptive Immunity; D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood; D025065:Borrelia burgdorferi / Q000276:immunology*; D018925:Chemokines / Q000097:blood; D016207:Cytokines / Q000097:blood; D003713:Dendritic Cells / Q000276:immunology / Q000378:metabolism; D004195:Disease Models, Animal; D006801:Humans; D008193:Lyme Disease / Q000276:immunology* / Q000382:microbiology; D008213:Lymphocyte Activation / Q000276:immunology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000172:deficiency* / Q000235:genetics / Q000276:immunology / Q000502:physiology; D016176:T-Lymphocyte Subsets / Q000276:immunology
chemical_list: D000907:Antibodies, Bacterial; D018925:Chemokines; D016207:Cytokines; D016692:Receptors, Antigen, T-Cell, gamma-delta