RESUMO
Intestinal T-cell lines were generated from lamina propria mononuclear cells isolated from colonoscopic biopsies in ulcerative colitis patients and controls. In both ulcerative colitis and controls, expanded cells were constituted largely by T-cell receptor alpha beta+, CD4+, CD45RA- (helper), and CD8+, CD11b- (cytotoxic) phenotypes. T-cell receptor V beta gene usage was not significantly changed after cell expansion and no difference was observed between ulcerative colitis and controls. Ulcerative colitis cells, especially those derived from the patients with long-standing disease, showed significantly higher levels of cytotoxicity against the target cells, including those of colonic epithelial origin, and enhanced production of tumor necrosis factor-alpha and interferon-gamma after short incubation with anti-CD3 antibody. Generation of T-cell lines from colonoscopic biopsy specimens may be useful for detailed functional characterization of locally infiltrating T cells in ulcerative colitis patients.
Assuntos
Biópsia , Colite Ulcerativa/imunologia , Colonoscopia , Mucosa Intestinal/citologia , Subpopulações de Linfócitos T , Adolescente , Adulto , Southern Blotting , Linhagem Celular , Colite Ulcerativa/patologia , Citotoxicidade Imunológica , Feminino , Citometria de Fluxo , Humanos , Interferon gama/biossíntese , Mucosa Intestinal/imunologia , Masculino , Pessoa de Meia-Idade , Receptores de Antígenos de Linfócitos T alfa-beta/análise , Receptores de Antígenos de Linfócitos T alfa-beta/genética , Linfócitos T/metabolismo , Fator de Necrose Tumoral alfa/biossínteseRESUMO
Phenotypic and functional analysis was performed with lamina propria mononuclear cells (LPMCs) isolated from colonoscopic biopsies in 27 patients with ulcerative colitis (UC). The proportion of T lymphocytes displaying HLA-DR antigens, interleukin 2 (IL-2) receptor, and transferrin receptor was greater in active UC than in control diseases. When LPMCs were cultured with IL-2 or phytohemagglutinin for 72 h, there were no significant differences in the proportion of cells bearing these activation markers between active UC and controls. The proportion of CD56+ cells and lymphokine-activated killer (LAK) cell activity was lower in LPMCs from active UC than in control cells, and depletion of CD56+ cells from control lamina propria cells essentially eliminated LAK cell activity. Mucosal T lymphocytes may be activated in vivo during active inflammation in UC, and lower levels of intestinal LAK cell activity may be related to the decrease of CD56+ cells under these conditions.
