title: Inducible bronchus-associated lymphoid tissue (iBALT) synergizes with local lymph nodes during antiviral CD4+ T cell responses.
abstract: BACKGROUND
  Exposure of the lungs to an antigen or pathogen elicits the formation of lymphoid satellite islands termed inducible bronchus-associated lymphoid tissue (iBALT). However, little is known about how the presence of iBALT, induced by a stimulus unrelated to the subsequent challenge agent, influences systemic immunity in distal locations, whether it be independently, antagonistically, or synergistically. Here, we determined the kinetics of the influenza-specific responses in the iBALT, tracheobronchial lymph node (TBLN), and spleen of mice with and without pre-formed iBALT.
  
  
  RESULTS
  Mice with VLP-induced iBALT or no pre-formed iBALT were challenged with influenza. We found that, as we have previously described, those mice whose lungs contained pre-formed iBALT were protected from morbidity, and furthermore, that these mice had increased dendritic cell, and alveolar macrophage accumulation in both the iBALT and TBLNs. This translated to similarly accelerated kinetics and intensified influenza-specific CD4(+), but not CD8(+) T cell responses in the iBALT, TBLN, and spleen. This expansion was then followed by a more rapid T cell contraction in all lymphoid tissues in the mice with pre-formed iBALT.
  
  
  CONCLUSIONS
  Thus, iBALT itself may not be responsible for the accelerated primary immune response we observe in mice with pre-formed iBALT, but may contribute to an overall accelerated local and systemic primary CD4(+), but not CD8(+) T cell response. Furthermore, less damaging immune responses observed in mice with pre-formed iBALT may be due to a quicker contraction of CD4(+) T cell responses in both local and systemic secondary lymphoid tissue.
authors.affiliation: 1 Department of Immunology and Infectious Diseases, Montana State University , Bozeman, Montana.
authors.forename: Laura E
authors.initials: LE
authors.lastname: Richert
authors.forename: Ann L
authors.initials: AL
authors.lastname: Harmsen
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Rynda-Apple
authors.forename: James A
authors.initials: JA
authors.lastname: Wiley
authors.forename: Amy E
authors.initials: AE
authors.lastname: Servid
authors.forename: Trevor
authors.initials: T
authors.lastname: Douglas
authors.forename: Allen G
authors.initials: AG
authors.lastname: Harmsen
mesh_terms: D000818:Animals; D001980:Bronchi / Q000276:immunology* / Q000473:pathology / Q000821:virology; D018791:CD4 Lymphocyte Count; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology* / Q000473:pathology / Q000821:virology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology / Q000473:pathology / Q000821:virology; D049109:Cell Proliferation; D020566:Dendritic Cells, Follicular / Q000276:immunology / Q000473:pathology / Q000821:virology; D005260:Female; D007111:Immunity, Cellular; D007113:Immunity, Innate; D053118:Influenza A Virus, H1N1 Subtype / Q000276:immunology; D008198:Lymph Nodes / Q000276:immunology* / Q000473:pathology / Q000821:virology; D008213:Lymphocyte Activation; D016676:Macrophages, Alveolar / Q000276:immunology / Q000473:pathology / Q000821:virology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009976:Orthomyxoviridae Infections / Q000276:immunology* / Q000473:pathology / Q000821:virology; D013154:Spleen / Q000276:immunology* / Q000473:pathology / Q000821:virology