Distribution of horseradish peroxidase (HRP)-anti-HRP immune complexes in mouse spleen with special reference to follicular dendritic cells.

Chen, Lei L.; Frank, Andrea M.; Adams, Judy; Steinman, Ralph M.

doi:10.1083/jcb.79.1.184

Cited by 84 publications

(40 citation statements)

References 27 publications

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“…An example of the latter is the retention of antigen-antibody complexes in the germinal center region of lymphoid organs. Chen et al (16), using horseradish peroxidase (HRP) as a marker, have shown that small amounts of HRP-anti-HRP immune complexes formed in antigen excess escape phagocytosis and instead associate with the cell surface of nonphagocytic follicular dendritic cells~ In this regard it is important to note that we have found that the mQst effective antigen presentation is performed by cells that are weakly phagocytic (Langerhans cells) or nonphagocytic (splenic dendritic cells, vide lhfra). (c) A third way of eliciting short-lived CS is by injecting the antigen-conjugated cells, that are predominantly macrophages, in such a way that primary immunization occurs in peripheral lymph nodes (3).…”

Section: Discussionmentioning

confidence: 99%

Role of antigen-presenting cells in the development and persistence of contact hypersensitivity.

Ptak¹,

Różycka²,

Askenase³

et al. 1980

The Journal of Experimental Medicine

156

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Three outcomes pertinent to contact sensitivity (CS) follow immunization with various forms of trinitrophenylated (TNP) substrates: (a) specific immunological unresponsiveness for CS is induced when immunization favors activation of splenic suppressor cells. This state is achieved by intravenous injection of trinitrophenyl-conjugated to various types of cells, such as peritoneal exudate cells (PEC). (b) A short-lived or evanescent form of CS is induced when immunization reduces activation of the suppressor circuit. This can be achieved by subcutaneous immunization with trinitrophenyl conjugated to syngeneic PEC, by pretreatment with cyclophosphamide to diminish suppression before intravenous immunization, or by altering the mode of antigen presentation by using TNP-substrate that has undergone phagocytosis. (c) A long-lived form of CS is induced when trinitrophenyl is presented to the immune system on skin cells either by contact skin painting with reactive trinitrophenyl, or by subcutaneous, or even intravenous injection of trinitrophenyl-conjugated epidermal cells. In fact, trinitrophenyl-conjugated epidermal cells induced CS even when the suppressor circuit was activated by intravenous coadministration of TNP-PEC. This implies that antigen presentation on epidermal cells induces sensitized cells that are relatively resistant to suppression. The cell type(s) in the skin that are primarily responsible for this potent form of antigen presentation are most likely Langerhans cells, because they can be concentrated by virtue of their Fc receptors and they are Ia positive. Thus, both the anatomical site where antigen is first encountered by the immune apparatus, as well as the nature of the cells which present the antigen, determine whether a CS response will ensue, as well as whether it will be evanescent or long-lasting.

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Section: Discussionmentioning

confidence: 99%

Role of antigen-presenting cells in the development and persistence of contact hypersensitivity.

Ptak¹,

Różycka²,

Askenase³

et al. 1980

The Journal of Experimental Medicine

156

View full text Add to dashboard Cite

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“…Spleens were removed next day, and the HRP Ag was detected by DAB histochemistry on cryosections. At this time point, FDCs in the GC region of the spleen are the only cell types with extracellular enzyme (17). ICs were readily trapped on FDCs in control mice (Fig.…”

Section: Lack Of Fdc Network and Ic Trapping In Relb-deficient Micementioning

confidence: 97%

“…For IC trapping, mice were immunized with SRBCs, and 6 days later injected i.v. with 200 g preformed peroxidase antiperoxidase ICs (Dako Diagnostika, Hamburg, Germany) (17). Spleens were removed 24 h later, embedded in Polyfreeze (Polysciences, Warrington, PA), and stored at Ϫ80°C.…”

Section: Immunizations and Ic Trappingmentioning

confidence: 99%

Essential Role of RelB in Germinal Center and Marginal Zone Formation and Proper Expression of Homing Chemokines

Weih

Yilmaz

Weih

2001

The Journal of Immunology

205

194

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High levels of the Rel/NF-κB family member RelB are restricted to specific regions of thymus, lymph nodes, and Peyer’s patches. In spleen, RelB is expressed in periarteriolar lymphatic sheaths, germinal centers (GCs), and the marginal zone (MZ). In this study, we report that RelB-deficient (relB−/−) mice, in contrast to nfkb1−/−, but similar to nfkb2−/− mice, are unable to form GCs and follicular dendritic cell networks upon Ag challenge in the spleen. RelB is also required for normal organization of the MZ and its population by macrophages and B cells. Reciprocal bone marrow transfers demonstrate that RelB expression in radiation-resistant stromal cells, but not in bone marrow-derived hemopoietic cells, is required for proper formation of GCs, follicular dendritic cell networks, and MZ structures. However, the generation of MZ B cells requires RelB in hemopoietic cells. Expression of TNF ligand/receptor family members is only moderately altered in relB−/− splenocytes. In contrast, expression of homing chemokines is strongly reduced in relB−/− spleen with particularly low mRNA levels of the chemokine B lymphocyte chemoattractant. Our data indicate that activation of p52-RelB heterodimers in stromal cells downstream of TNF/lymphotoxin is required for normal expression of homing chemokines and proper development of spleen microarchitecture.

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“…For immune stimulation, we treated mice with either preformed immune complexes (ICs) of HRP and mouse-monoclonal anti-HRP IgG, or vesicular stomatitis virus (VSV), a member of the Rhabdoviridae family. Treatment with preformed ICs has been reported to lead to IC trapping on the surface of FDCs and presentation to germinal center B cells (14). An infection with VSV, in contrast, is defeated primarily by a neutralizing IgM response, but also elicits a germinal center reaction that is characterized by longtime persistence of VSV Ag on FDCs and the maintenance of a memory IgG titer (15).…”

mentioning

confidence: 99%

Immunologically Induced, Complement-Dependent Up-Regulation of the Prion Protein in the Mouse Spleen: Follicular Dendritic Cells Versus Capsule and Trabeculae

Lötscher

Recher²,

Hunziker³

et al. 2003

The Journal of Immunology

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The expression of the prion protein (PrP) in the follicular dendritic cell network of germinal centers in the spleen is critical for the splenic propagation of the causative agent of prion diseases. However, a physiological role of the prion protein in the periphery remains elusive. To investigate the role and function of PrP expression in the lymphoid system we treated naive mice i.v. with preformed immune complexes or vesicular stomatitis virus. Immunohistochemistry and Western blot analysis of the spleen revealed that 8 days after immunization, immune complexes and vesicular stomatitis virus had both induced a strong increase of PrP expression in the follicular dendritic cell network. Remarkably, this up-regulation did not occur in mice that lack an early factor of the complement cascade, C1q, a component which has been shown previously to facilitate early prion pathogenesis. In addition to the variable PrP level in the germinal centers, we detected steady and abundant PrP expression in the splenic capsule and trabeculae, which are structural elements that have not been associated before with PrP localization. The abundant trabeculo-capsular PrP expression was also evident in spleens of Rag-1-deficient mice, which have been shown before to be incapable of prion expansion. We conclude that trabeculocapsular PrP is not sufficient for splenic prion propagation. Furthermore, our observations may provide important clues for a physiological function of the prion protein and allow a new view on the role of complement and PrP in peripheral prion pathogenesis.

show abstract

Distribution of horseradish peroxidase (HRP)-anti-HRP immune complexes in mouse spleen with special reference to follicular dendritic cells.

Cited by 84 publications

References 27 publications

Role of antigen-presenting cells in the development and persistence of contact hypersensitivity.

Role of antigen-presenting cells in the development and persistence of contact hypersensitivity.

Essential Role of RelB in Germinal Center and Marginal Zone Formation and Proper Expression of Homing Chemokines

Immunologically Induced, Complement-Dependent Up-Regulation of the Prion Protein in the Mouse Spleen: Follicular Dendritic Cells Versus Capsule and Trabeculae

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