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Titolo:
EVIDENCE THAT CD4(-CELLS ARE RESPONSIBLE FOR MURINE INTERLEUKIN-2-DEFICIENT COLITIS(), BUT NOT CD8(+) T)
Autore:
SIMPSON SJ; MIZOGUCHI E; ALLEN D; BHAN AK; TERHORST C;
Indirizzi:
HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DIV IMMUNOL,330 BROOKLINE AVE BOSTON MA 02215 HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DIV IMMUNOL BOSTON MA 02215 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL BOSTON MA 00000
Titolo Testata:
European Journal of Immunology
fascicolo: 9, volume: 25, anno: 1995,
pagine: 2618 - 2625
SICI:
0014-2980(1995)25:9<2618:ETCARF>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
INFLAMMATORY BOWEL-DISEASE; CHRONIC INTESTINAL INFLAMMATION; RECEPTOR MUTANT MICE; INTRAEPITHELIAL LYMPHOCYTES; EPITHELIAL-CELLS; ULCERATIVE-COLITIS; GUT; ANTIGEN; DIFFERENTIATION; EXPRESSION;
Keywords:
CD4(+) T CELL; ULCERATIVE COLITIS; CYTOTOXIC T CELL;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
43
Recensione:
Indirizzi per estratti:
Citazione:
S.J. Simpson et al., "EVIDENCE THAT CD4(-CELLS ARE RESPONSIBLE FOR MURINE INTERLEUKIN-2-DEFICIENT COLITIS(), BUT NOT CD8(+) T)", European Journal of Immunology, 25(9), 1995, pp. 2618-2625

Abstract

Mice deficient in interleukin-2 production (IL-2(null) mice) develop colonic inflammation closely resembling ulcerative colitis in humans. Although this disease is marked by substantial infiltration of the colon by CD8(+) and CD4(+) T lymphocytes, no function has yet been assigned to these T cell subsets in the development of colitis in the IL-2(null) mouse. For the present study, we investigated the involvement of T lymphocytes in the onset of colitis in IL-2(null) mice, and examinedthe possible role played by cytotoxic T cells. Both lamina propria lymphocytes (LPL) and intraepithelial lymphocytes (IEL) of the colon of IL-2(null) mice were potently cytotoxic ex vivo in short-term redirected cytotoxic lymphocyte (CTL) assays. In contrast, colonic T cells of wild-type animals showed little or no constitutive cytotoxic T cell activity. Colonic CTL were detectable prior to the appearance of diseasein IL-2(null) animals and CTL activity was confined to the TcR alpha beta, rather than to the TcR gamma delta TEL subset. IL-2(null) animals crossed with major histocompatibility complex class I-deficient mice[IL-2(null) x beta(2) microglobulin (beta(2)m(null)) mice] also developed colitis, which appeared even earlier than in most IL-2(null) mice. These findings suggest that neither CD8(+) IEL nor LPL were causal in the onset of colitis in IL-2(null) animals. In IL-2(null) x beta(2)m(null) mice, an ulcerative colitis-like disease was evident from histological studies and immunohistological staining which showed very large numbers of CD4(+) lymphocytes within the intestinal mucosa. Significant ex vivo killing by CD4(+) T cells was observed in IL-2(null) x beta(2)m(null) animals, although this required an extended incubation time compared to colonic CD8(+) T cells. Peripheral as well as colonic CD4(+) T cells in IL-2(null) and IL-2(null) x beta(2)m(null) animals, were activated as judged by their cell surface phenotype (CD45RB(lo), L-selectin(lo) and CD69(+)). In light of these findings, we propose thatinfiltrating CD4(+), but not CD8(+) T cells are central to the inflammation observed in the intestinal mucosa in IL-2(null) colitis.

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Documento generato il 22/09/20 alle ore 05:44:18