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| Untersuchte Arbeit: Seite: 8, Zeilen: 1-9 |
Quelle: Lipscomb and Masten 2002 Seite(n): 116, Zeilen: right col. 17-30 |
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| [Active suppression of immature DC maturation by alveolar macrophages may explain why airway and] intraepithelial DC remain immature during their steady-state migration to lung-associated lymph nodes (Holt, 1993; Lipscomb et al., 1993). Furthermore, autocrine production of IL-10 by immature DC can inhibit surface expression of MHC class-I and -II molecules and exert a generalized inhibitory effect on T cell proliferation (Stumbles et al., 1998). On exposure to inhaled allergens, the antigen may simply be insufficient in providing a danger signal to overcome suppression by alveolar macrophages and IL-10. However, if a danger signal is present at the tissue site, DC mature and migrate in greater number to draining lymph nodes to stimulate CD4+ T cell clonal expansion and differentiation.
Holt PG. Development of bronchus associated lymphoid tissue (BALT) in human lung disease: a normal host defence mechanism awaiting therapeutic exploitation? Thorax. 1993 Nov; 48 (11): 1097-8. Holt PG. Pulmonary dendritic cell populations. Adv Exp Med Biol. 1993; 329: 557-62. Review. Lipscomb MF, Pollard AM, Yates JL. A role for TGF-beta in the suppression by murine bronchoalveolar cells of lung dendritic cell initiated immune responses. Reg Immunol. 1993 May-Aug; 5 (3-4): 151-7. Stumbles PA, Thomas JA, Pimm CL, Lee PT, Venaille TJ, Proksch S, Holt PG. Resting respiratory tract dendritic cells preferentially stimulate T helper cell type 2 (Th2) responses and require obligatory cytokine signals for induction of Th1 immunity. J Exp Med. 1998 Dec 7; 188 (11): 2019-31. |
Active suppression of immature DC maturation by alveolar macrophages may explain why airway and intraepithelial DCs remain immature during their steady-state migration to lung-associated lymph nodes (LALNs) (141, 203). Furthermore, autocrine production of IL-10 by immature DCs can inhibit surface expression of MHC class II and exert a generalized inhibitory effect on T cell proliferation (238, 334). On exposure to inhaled allergens, the antigen may simply be insufficient in providing a danger signal to overcome suppression by alveolar macrophages and IL-10. However, if a danger signal is present at the tissue site, DCs mature and migrate in greater numbers to the draining lymph nodes to stimulate CD4 T cell clonal expansion and differentiation.
141. HOLT PG. Macrophage: dendritic cell interaction in regulation of IgE response in asthma. Clin Exp Allergy 23: 4–6, 1993. 203. LIPSCOMB MF, POLLARD AM, AND YATES JL. A role for TGF-beta in the suppression by murine bronchoalveolar cells of lung dendritic cell initiated immune responses. Reg Immunol 5: 151–157, 1993. 238. MOORE KW, O’GARRA A, DE WAAL MALEFYT R, VIEIRA P, AND MOSMANN TR. Interleukin-10. Annu Rev Immunol 11: 165–190, 1993. 334. STUMBLES PA, THOMAS JA, PIMM CL, LEE PT, VENAILLE TJ, PROKSCH S, AND HOLT PG. Resting respiratory tract dendritic cells preferentially stimulate T helper cell type 2 (Th2) responses and require obligatory cytokine signals for induction of Th1 immunity. J Exp Med 188: 2019–2031, 1998. |
Largely identical, without any part of it marked as a citation. No source given. |
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