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Graf Isolan
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Untersuchte Arbeit:
Seite: 12, Zeilen: 15-17, 19-36
Quelle: Niess 2008
Seite(n): 5138, 5144, Zeilen: 5138:li.Sp. 24-32; re.Sp. 3-21.24ff; 5144:li.Sp. 11-14
1.9. Mucosal dendritic cells

Mucosal DCs are assumed to play key roles in regulating immune responses in the antigen-rich gastrointestinal environment. [...] Mucosal DCs are a heterogeneous population that can either initiate (innate and adaptive) immune responses, or control intestinal inflammation and maintain tolerance (Nagler-Anderson 2001; Steinman and Nussenzweig 2002b).

The intestinal innate and adaptive immune system has evolved in response to potent stimuli derived from constituents of the commensal microflora. In most cases these local immune responses achieve tolerance to the intestinal microflora and food antigens. Tolerance to intestinal self antigens, oral antigens and the commensal flora is achieved by interactions of DCs with regulatory and effector T cells. Local T cell immunity is an important compartment of the specific intestinal immune system. T cell reactivity is programmed during the initial stage of its activation by DCs (Medzhitov and Janeway, Jr. 1999).

DCs reside in mucosal tissues or recirculate in the blood and lymphoid tissues (Iwasaki 2007). The lamina propria of the small and large intestine are effector sites of mucosal tissues. The local microenvironment influences the phenotype of DCs, and are characterized by a remarkable plasticity between DCs (Kelsall and Rescigno 2004). In the lamina propria of the small and large intestine, DCs are ideally situated to survey the constituents of the commensal microflora and monitor food antigens (Bjorck 2001).

Defects in this regulation are supposed to lead to the several forms of inflammatory disease such as: Crohn's disease (CD) and ulcerative colitis (UC) (MacDonald and Monteleone 2005) [and hemorrhagic rectocolitis (HRC), a deregulation of the intestinal immune system would lead to an inadequate response against one or more endoluminal antigens.]


Bjorck,P., 2001. Isolation and characterization of plasmacytoid dendritic cells from Flt3 ligand and granulocyte-macrophage colony-stimulating factor-treated mice. Blood 98, 3520-3526.

Iwasaki,A., 2007. Mucosal dendritic cells. Annu. Rev. Immunol. 25, 381-418.

Kelsall,B.L., Rescigno,M., 2004. Mucosal dendritic cells in immunity and inflammation. Nat. Immunol. 5, 1091-1095.

MacDonald,T.T., Monteleone,G., 2005. Immunity, inflammation, and allergy in the gut. Science 307, 1920-1925.

Medzhitov,R., Janeway,C.A., Jr., 1999. Innate immune induction of the adaptive immune response. Cold Spring Harb. Symp. Quant. Biol. 64, 429-435.

Nagler-Anderson,C., 2001. Man the barrier! Strategic defences in the intestinal mucosa. Nat. Rev. Immunol. 1, 59-67.

[Seite 5138]

Abstract

[...] Mucosal dendritic cells (DCs) are assumed to play key roles in regulating immune responses in the antigen-rich gastrointestinal environment. Mucosal DCs are a heterogeneous population that can either initiate (innate and adaptive) immune responses, or control intestinal inflammation and maintain tolerance. Defects in this regulation are supposed to lead to the two major forms of inflammatory bowel disease (IBD), Crohn’s disease (CD) and ulcerative colitis (UC). [...] The local microenvironment influences the phenotype of DCs, a heterogeneous population that can be divided into conventional DCs (CD8α+CD11b-, CD4+CD11b+, CD4-CD11b+)[7,8] and plasmacytoid DCs (B220+CD11clow) (Table 2) and are characterized by a remarkable plasticity between DCs[9]. In the lamina propria of the small and large intestine, DCs are ideally situated to survey the constituents of the commensal microflora and monitor food antigens[10].

[...]

INTRODUCTION

The intestinal innate and adaptive immune system has evolved in response to potent stimuli derived from constituents of the commensal microflora. In most cases these local immune responses achieve tolerance to the intestinal microflora and food antigens. Defects of the tightly regulated mucosal immune responses are assumed to result in inflammatory bowel disease (IBD), such as Crohn’s disease (CD) and ulcerative colitis (UC)[1,2]. Local T cell immunity is an important compartment of the specific intestinal immune system. T cell reactivity is programmed during the initial stage of its activation by dendritic cells (DCs) that can either initiate (innate and adaptive) immune responses, or control intestinal inflammation and maintain tolerance[3-5].DCs reside in mucosal tissues or recirculate in the blood and lymphoid tissues[6]. The lamina propria of the small and large intestine are effector sites of mucosal tissues.

[Seite 5144]

CONCLUSION

[...] Tolerance to intestinal self antigens, oral antigens and the commensal flora is achieved by interactions of DCs with regulatory and effector T cells.


1 Xavier RJ, Podolsky DK. Unravelling the pathogenesis of inflammatory bowel disease. Nature 2007; 448: 427-434

2 Strober W. Immunology. Unraveling gut inflammation. Science 2006; 313: 1052-1054

3 Nagler-Anderson C. Man the barrier! Strategic defences in the intestinal mucosa. Nat Rev Immunol 2001; 1: 59-67

4 Niess JH, Reinecker HC. Dendritic cells in the recognition of intestinal microbiota. Cell Microbiol 2006; 8: 558-564

5 Steinman RM, Nussenzweig MC. Avoiding horror autotoxicus: the importance of dendritic cells in peripheral T cell tolerance. Proc Natl Acad Sci US 2002; 99: 351-358

6 Iwasaki A. Mucosal dendritic cells. Annu Rev Immunol 2007; 25: 381-418

7 Vremec D, Shortman K. Dendritic cell subtypes in mouse lymphoid organs: cross-correlation of surface markers, changes with incubation, and differences among thymus, spleen, and lymph nodes. J Immunol 1997; 159: 565-573

8 Hochrein H, Shortman K, Vremec D, Scott B, Hertzog P, O'Keeffe M. Differential production of IL-12, IFN-alpha, and IFN-gamma by mouse dendritic cell subsets. J Immunol 2001; 166: 5448-5455

9 Kelsall BL, Rescigno M. Mucosal dendritic cells in immunity and inflammation. Nat Immunol 2004; 5: 1091-1095

10 Bjorck P. Isolation and characterization of plasmacytoid dendritic cells from Flt3 ligand and granulocytemacrophage colony-stimulating factor-treated mice. Blood 2001; 98: 3520-3526

Anmerkungen

Im Literaturverzeichnis findet sich keine Referenz für Steinman and Nussenzweig (2002b).

Auf der Folgeseite, wo noch ein Absatz folgt, der nicht aus Niess (2008), sondern aus Delcenserie et al (2008) stammt (vgl. Ntx/Fragment_013_01) wird die Quelle am Ende dieses Absatzes (endlich) genannt.

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