title: Early immune activation in gut-associated and peripheral lymphoid tissue during acute HIV infection.
abstract: OBJECTIVE
  To study innate and adaptive immune responses in gut-associated lymphoid tissue (GALT) as well as peripheral lymphoid tissue (pLT) obtained from individuals with acute HIV-1 infection syndrome.
  
  
  METHODS
  The expression of chemokines [regulated upon activation: normal T cell expressed/secreted (RANTES), macrophage-inflammatory protein (MIP) 1alpha/beta], cytokines (IL-1beta, TNF-alpha, IL-12, IL-4, IL-10, IL-2, IFN-gamma) and cytotoxic effector molecules (granzyme A, perforin) and cell marker (CD8) were analysed at the single cell level in GALT and pLT of patients experiencing acute HIV-1 infection (day -3 to 48 days from onset of acute symptoms).
  
  
  RESULTS
  Substantial pro-inflammatory immune responses (TNF-alpha, IL-1beta, IL-12) and expansion in the CD8 T-cell population were noted in both compartments compared with uninfected controls. This was associated with an early increased expression of beta-chemokines (RANTES, MIP-1alpha/beta) and granzyme, but not with an increase in the expression of perforin. The upregulation of IL-2, IL-12 and IL-4 was noted in both pLT and GALT, whereas IL-10 expression was mainly increased in GALT.
  
  
  CONCLUSIONS
  Taken together, these findings demonstrate that there was a broad and early immune activation in GALT and pLT during acute HIV-1 infection. The relative lack of perforin expression in both GALT and pLT, however, questions the functional efficacy of the observed immune activation in generating cytotoxic T cells that were able to eliminate HIV-infected cells.
authors.affiliation: Center for Infectious Medicine and Division of Infectious Diseases, Karolinska University Hospital, Karolinska Institutet, Huddinge, Stockholm, Sweden. j.nilsson@ki.se
authors.forename: Jakob
authors.initials: J
authors.lastname: Nilsson
authors.forename: Sabine
authors.initials: S
authors.lastname: Kinloch-de-Loes
authors.forename: Anna
authors.initials: A
authors.lastname: Granath
authors.forename: Anders
authors.initials: A
authors.lastname: Sönnerborg
authors.forename: Li-Ean
authors.initials: LE
authors.lastname: Goh
authors.forename: Jan
authors.initials: J
authors.lastname: Andersson
mesh_terms: D000208:Acute Disease; D000328:Adult; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5 / Q000378:metabolism; D003106:Colon / Q000276:immunology*; D016207:Cytokines / Q000378:metabolism; D015658:HIV Infections / Q000276:immunology*; D015497:HIV-1; D006801:Humans; D007111:Immunity, Cellular; D018836:Inflammation Mediators / Q000378:metabolism; D007378:Interleukins / Q000378:metabolism; D008213:Lymphocyte Activation / Q000276:immunology; D008221:Lymphoid Tissue / Q000276:immunology*; D019402:Macrophage Inflammatory Proteins / Q000378:metabolism; D008297:Male; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
chemical_list: D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5; D016207:Cytokines; D018836:Inflammation Mediators; D007378:Interleukins; D019402:Macrophage Inflammatory Proteins