title: Peritoneal T lymphocyte regulation by macrophages.
abstract: The T cell composition of the peritoneal cavity (PerC) in naïve BALB/c, C57BL/6, DBA/2J, and B-1 B cell-defective BALB.xid mice was investigated. The BALB.xid PerC T cell pool had a high CD4:CD8 T cell ratio relative to the other strains whose ratios were similar to those found in their lymph node and spleen. All mice had significant representation of T cells with an activated (CD25(+), GITR(hi), CD44(hi), CD45RB(lo), CD62L(lo)) phenotype and low numbers of Foxp3(+) T(reg) cells in their PerC. Despite a phenotype indicative of activation, peritoneal T cell responses to CD3 ligation were very low for C57BL/6 and BALB.xid, but not BALB/c, mice. Enzyme inhibition and cytokine neutralization studies revealed active suppression of the T cell response mediated by the macrophages that represent a significant portion of PerC leucocytes. Driven by IFNγ to express iNOS, macrophages suppressed T cell activation in vitro by arginine catabolism. Although BALB/c T cells were also in a macrophage-dense environment their limited IFNγ production failed to trigger suppression. This difference between BALB/c and BALB.xid PerC T cells suggests a role for xid in shaping macrophage-mediated immune regulation.
authors.affiliation: Department of Biology, Rider University, Lawrenceville, NJ 08648-3099, USA.
authors.forename: G
authors.initials: G
authors.lastname: Composto
authors.forename: D
authors.initials: D
authors.lastname: Gonzalez
authors.forename: A
authors.initials: A
authors.lastname: Bucknum
authors.forename: D
authors.initials: D
authors.lastname: Silberman
authors.forename: J
authors.initials: J
authors.lastname: Taylor
authors.forename: M
authors.initials: M
authors.lastname: Kozlowski
authors.forename: T
authors.initials: T
authors.lastname: Bloomfield
authors.forename: T
authors.initials: T
authors.lastname: Bartlett
authors.forename: J
authors.initials: J
authors.lastname: Riggs
mesh_terms: D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D002450:Cell Communication / Q000276:immunology; D002478:Cells, Cultured; D051858:Forkhead Transcription Factors / Q000096:biosynthesis; D053450:Glucocorticoid-Induced TNFR-Related Protein; D007108:Immune Tolerance; D007156:Immunologic Memory; D053645:Interleukin-2 Receptor alpha Subunit / Q000096:biosynthesis; D017737:Macrophages, Peritoneal / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D008815:Mice, Inbred Strains; D008817:Mice, Mutant Strains; D017475:Receptors, Nerve Growth Factor / Q000096:biosynthesis; D018124:Receptors, Tumor Necrosis Factor / Q000096:biosynthesis; D050378:T-Lymphocytes, Regulatory / Q000276:immunology / Q000378:metabolism* / Q000473:pathology
chemical_list: D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse; D053450:Glucocorticoid-Induced TNFR-Related Protein; D053645:Interleukin-2 Receptor alpha Subunit; D017475:Receptors, Nerve Growth Factor; D018124:Receptors, Tumor Necrosis Factor; C106544:Tnfrsf18 protein, mouse