scholarly journals Peripheral CD103+ dendritic cells form a unified subset developmentally related to CD8α+ conventional dendritic cells

2010 ◽  
Vol 207 (4) ◽  
pp. 823-836 ◽  
Author(s):  
Brian T. Edelson ◽  
Wumesh KC ◽  
Richard Juang ◽  
Masako Kohyama ◽  
Loralyn A. Benoit ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Transcription Factor ◽  
Lymph Nodes ◽  
Sendai Virus ◽  
Pulmonary Inflammation ◽  
Lymphoid Organ ◽  
Contact Hypersensitivity ◽  
Lymphoid Tissues ◽  
Mesenteric Lymph Nodes ◽  
Normal Contact

Although CD103-expressing dendritic cells (DCs) are widely present in nonlymphoid tissues, the transcription factors controlling their development and their relationship to other DC subsets remain unclear. Mice lacking the transcription factor Batf3 have a defect in the development of CD8α+ conventional DCs (cDCs) within lymphoid tissues. We demonstrate that Batf3−/− mice also lack CD103+CD11b− DCs in the lung, intestine, mesenteric lymph nodes (MLNs), dermis, and skin-draining lymph nodes. Notably, Batf3−/− mice displayed reduced priming of CD8 T cells after pulmonary Sendai virus infection, with increased pulmonary inflammation. In the MLNs and intestine, Batf3 deficiency resulted in the specific lack of CD103+CD11b− DCs, with the population of CD103+CD11b+ DCs remaining intact. Batf3−/− mice showed no evidence of spontaneous gastrointestinal inflammation and had a normal contact hypersensitivity (CHS) response, despite previous suggestions that CD103+ DCs were required for immune homeostasis in the gut and CHS. The relationship between CD8α+ cDCs and nonlymphoid CD103+ DCs implied by their shared dependence on Batf3 was further supported by similar patterns of gene expression and their shared developmental dependence on the transcription factor Irf8. These data provide evidence for a developmental relationship between lymphoid organ–resident CD8α+ cDCs and nonlymphoid CD103+ DCs.

In situ demonstration of migration of dendritic cells released from rat small intestine to mesenteric lymph nodes

2001 ◽  
Vol 120 (5) ◽  
pp. A183-A183
Author(s):  
H KOBAYASHI ◽  
H NAGATA ◽  
S MIURA ◽  
T AZUMA ◽  
H SUZUKI ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Small Intestine ◽  
Lymph Nodes ◽  
Rat Small Intestine ◽  
Mesenteric Lymph Nodes ◽  
Mesenteric Lymph

scholarly journals Quantitative analysis of total macrophage content in adult mouse tissues. Immunochemical studies with monoclonal antibody F4/80.

1985 ◽  
Vol 161 (3) ◽  
pp. 475-489 ◽  
Author(s):  
S H Lee ◽  
P M Starkey ◽  
S Gordon
Keyword(s):  
Bone Marrow ◽  
Small Bowel ◽  
Lymph Nodes ◽  
Large Bowel ◽  
Adult Mouse ◽  
Specific Antigen ◽  
Lymphoid Tissues ◽  
Mesenteric Lymph Nodes ◽  
Mesenteric Lymph ◽  
Mouse Tissues

We have estimated the macrophage content of different tissues of the normal adult mouse using F4/80, a highly specific antigen marker for mature mouse macrophages. An absorption indirect binding assay was used to quantitate F4/80 antigen against a calibration standard made from the J774.2 macrophage-like cell line. The richest sources of tissue F4/80 antigen were found to be bone marrow, spleen, cervical and mesenteric lymph nodes, large bowel, liver, kidneys, and small bowel. The organs that have the highest total F4/80 antigen content are the liver, large bowel, small bowel, bone marrow, spleen, cervical and mesenteric lymph nodes, and kidney. We conclude that the mononuclear phagocyte system is mainly distributed in the gastrointestinal tract and liver, followed by hemopoietic and lymphoid tissues.

scholarly journals Altered ratio of dendritic cell subsets in skin-draining lymph nodes promotes Th2-driven contact hypersensitivity

2021 ◽  
Vol 118 (3) ◽  
pp. e2021364118
Author(s):  
Hannah L. Miller ◽  
Prabhakar Sairam Andhey ◽  
Melissa K. Swiecki ◽  
Bruce A. Rosa ◽  
Konstantin Zaitsev ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Lymph Nodes ◽  
Diphtheria Toxin ◽  
Fluorescein Isothiocyanate ◽  
Skin Inflammation ◽  
Contact Hypersensitivity ◽  
Type I ◽  
Th2 Response ◽  
Draining Lymph Nodes

Plasmacytoid dendritic cells (pDCs) specialize in the production of type I IFN (IFN-I). pDCs can be depleted in vivo by injecting diphtheria toxin (DT) in a mouse in which pDCs express a diphtheria toxin receptor (DTR) transgene driven by the human CLEC4C promoter. This promoter is enriched for binding sites for TCF4, a transcription factor that promotes pDC differentiation and expression of pDC markers, including CLEC4C. Here, we found that injection of DT in CLEC4C-DTR+ mice markedly augmented Th2-dependent skin inflammation in a model of contact hypersensitivity (CHS) induced by the hapten fluorescein isothiocyanate. Unexpectedly, this biased Th2 response was independent of reduced IFN-I accompanying pDC depletion. In fact, DT treatment altered the representation of conventional dendritic cells (cDCs) in the skin-draining lymph nodes during the sensitization phase of CHS; there were fewer Th1-priming CD326+ CD103+ cDC1 and more Th2-priming CD11b+ cDC2. Single-cell RNA-sequencing of CLEC4C-DTR+ cDCs revealed that CD326+ DCs, like pDCs, expressed DTR and were depleted together with pDCs by DT treatment. Since CD326+ DCs did not express Tcf4, DTR expression might be driven by yet-undefined transcription factors activating the CLEC4C promoter. These results demonstrate that altered DC representation in the skin-draining lymph nodes during sensitization to allergens can cause Th2-driven CHS.

scholarly journals Global vascular expression of murine CD34, a sialomucin-like endothelial ligand for L-selectin

Blood ◽  
1994 ◽  
Vol 84 (8) ◽  
pp. 2554-2565 ◽  
Author(s):  
S Baumhueter ◽  
N Dybdal ◽  
C Kyle ◽  
LA Lasky
Keyword(s):  
Lymph Nodes ◽  
Immune Surveillance ◽  
Nod Mice ◽  
Lymphoid Tissues ◽  
Mesenteric Lymph Nodes ◽  
High Endothelial Venules ◽  
Endothelial Cell Surface ◽  
Vascular Expression

Abstract Extravasation of leukocytes into organized lymphoid tissues and into sites of inflammation is critical to immune surveillance. Leukocyte migration to peripheral lymph nodes (PLN), mesenteric lymph nodes (MLN) and Peyer's patches (PP) depends on L-selectin, which recognizes carbohydrate-bearing, sialomucin-like endothelial cell surface glycoproteins. Two of these ligands have been identified at the molecular level. One is the potentially soluble mucin, GlyCAM 1, which is almost exclusively produced by high endothelial venules (HEV) of PLN and MLN. The second HEV ligand for L-selectin is the membrane-bound sialomucin CD34. Historically, this molecule has been successfully used to purify human pluripotent bone marrow stem cells, and limited data suggest that human CD34 is present on the vascular endothelium of several organs. Here we describe a comprehensive analysis of the vascular expression of CD34 in murine tissues using a highly specific antimurine CD34 polyclonal antibody. CD34 was detected on vessels in all organs examined and was expressed during pancreatic and skin inflammatory episodes. A subset of HEV-like vessels in the inflamed pancreas of nonobese diabetic (NOD) mice are positive for both CD34 and GlyCAM 1, and bind to an L-selectin/immunoglobulin G (IgG) chimeric probe. Finally, we found that CD34 is present on vessels of deafferentiated PLN, despite the fact that these vessels are no longer able to interact with L-selectin or support lymphocyte binding in vitro or trafficking in vivo. Our data suggest that the regulation of posttranslational carbohydrate modifications of CD34 is critical in determining its capability to act as an L-selectin ligand. Based on its ubiquitous expression, we propose that an appropriately glycosylated form of vascular CD34 may act as a ligand for L-selectin-mediated leukocyte trafficking to both lymphoid and nonlymphoid sites.

scholarly journals Studies on the pathogenesis of rinderpest in experimental cattle: III. Proliferation of an attenuated strain in various tissues following subcutaneous inoculation

1965 ◽  
Vol 63 (2) ◽  
pp. 263-275 ◽  
Author(s):  
W. P. Taylor ◽  
W. Plowright
Keyword(s):  
Lymph Nodes ◽  
Subcutaneous Tissue ◽  
Neutralizing Antibody ◽  
Vaccine Virus ◽  
Lymphoid Tissues ◽  
Mesenteric Lymph Nodes ◽  
Serum Samples ◽  
Virulent Strains ◽  
Eclipse Phase ◽  
Subcutaneous Inoculation

Twenty-five grade cattle were infected subcutaneously with 1040 to 104·6 TCD 50 of a highly-attenuated strain of rinderpest virus which is used as a vaccine. No clinical reaction was observed but the proliferation of virus was studied in twenty-two tissues harvested at daily intervals from the first to the 10th days after inoculation. Serum samples collected at the same times were examined for rinderpest-neutralizing antibody.There was an ‘eclipse’ phase of 3 days during which no infectivity could be demonstrated in any tissue. On the 4th day virus had generalized, as shown by its detection in lymphoid tissues which were not associated with the site of inoculation; occasional animals showed evidence of viral proliferation in the local muscle and subcutaneous tissue. A considerable growth of virus, with peak titres between 104·0 and 105·0 TDC50/g., was demonstrated in the prescapular, pharyngeal and mesenteric lymph nodes, also in the palatal tonsils and Peyer's patches of the ileum. Highest titres (105·4 TCD50/g.) were recorded in the prescapular haemo-lymph nodes, but less virus (up to 103·4 TCD50/g.) appeared in the spleen.A low-level viraemia was detected in eight of the thirteen cattle killed on the 5th to 8th days inclusive. Minimal quantities of virus were found on two occasions each in the bone marrow and lung. No virus was recovered from the mucosae of the base of the tongue, abomasum, ileum, caecum and colon; liver, heart, kidney and brain tissue also failed to support its multiplication.Neutralizing antibody was present in all cattle by the 10th day after inoculation, its appearance being associated with the abrupt decline in virus titres, which was usually demonstrable on the 8th day.The behaviour of the attenuated virus was compared with that of virulent strains, and it was concluded that its lack of pathogenicity was due primarily to its failure to proliferate in the mucosae of the gastro-intestinal and respiratory tracts. Vaccine virus was, in fact, exclusively ‘lymphotropic’, a characteristic which may account for the solid, lasting immunity it confers and for the considerable antibody response it provokes in inoculated cattle. Inability to spread by contact amongst susceptible cattle may be a result of the absence of virus in mucosae or parenchymatous organs and hence in excretions.

scholarly journals ANTIBODIES OF THE IgA TYPE IN INTESTINAL PLASMA CELLS OF GERMFREE MICE AFTER ORAL OR PARENTERAL IMMUNIZATION WITH FERRITIN

1969 ◽  
Vol 130 (4) ◽  
pp. 723-744 ◽  
Author(s):  
P. A. Crabbé ◽  
D. R. Nash ◽  
H. Bazin ◽  
H. Eyssen ◽  
J. F. Heremans
Keyword(s):  
Lymph Nodes ◽  
Plasma Cells ◽  
Lymphoid Tissues ◽  
Mesenteric Lymph Nodes ◽  
Repeated Stimulation ◽  
C3h Mice ◽  
Parenteral Immunization ◽  
Circulating Antibodies ◽  
A Site ◽  
Horse Spleen Ferritin

In adult germfree C3H mice immunized with horse spleen ferritin, either subcutaneously or intraperitoneally, plasma cells containing specific antibodies were found in lymph nodes and spleen and, in smaller numbers, also in the lamina propria of the intestine. In extraintestinal sites, these antiferritin-containing plasma cells were mainly of the IgM class after a single stimulation, and of the IgG1 class after repeated stimulation. In the intestine, all the anti-ferritin-containing cells appeared to be of the IgA class. Circulating antibodies, after repeated stimulation, were for the major part IgG1 and IgG2. In germfree mice given ferritin in their drinking water, antiferritin-containing cells were abundant in the intestinal mucosa, much less numerous in the mesenteric lymph nodes, and extremely scarce in other lymphoid tissues. All these cells, whatever their location, appeared to belong exclusively to the IgA class. Similarly, all the circulating antibody in these animals was found to be IgA. These findings illustrate the role of the gut as a site of antibody synthesis, as well as its selective commitment to the production of antibodies of the IgA class.

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