scholarly journals In vitro alteration of receptors for vasoactive intestinal peptide changes the in vivo localization of mouse T cells.

1984 ◽  
Vol 160 (4) ◽  
pp. 1054-1069 ◽  
Author(s):  
C A Ottaway
Keyword(s):  
T Cells ◽  
Vasoactive Intestinal Peptide ◽  
Receptor Expression ◽  
Peyer's Patches ◽  
Peyer’S Patches ◽  
Mesenteric Lymph Nodes ◽  
Dose Dependent Decrease ◽  
Dose Dependent

The capacity of T lymphocytes exposed in vitro to the neuropeptide vasoactive intestinal peptide (VIP) to bind VIP in vitro and to migrate to different tissues in vivo has been studied. VIP treatment of T cells resulted in a time- and dose-dependent loss of the ability of T cells to specifically bind radioiodinated VIP. Altered binding was due to a decrease in the expression of cellular receptors for VIP on the treated cells rather than an alteration in the affinity of the cells for the neuropeptide. Alteration of VIP receptor expression was not associated with a change in the expression of Thy-1, Lyt-1, or Lyt-2 surface markers by the treated cells. VIP treatment of T cells in vitro resulted, however, in a dose-dependent decrease in the ability of the treated cells to localize in mesenteric lymph nodes (MLN) and Peyer's patches of recipient animals at early times after cell transfer, and this was due to a selective decrease in the rate of accumulation of the treated cells in these tissues. There was no alteration in the distribution of VIP-treated cells in the blood, spleen, liver, or other major organs of the recipient animals. It is concluded that the presence of VIP receptors on T cells facilitates the entry of T cells into MLN and Peyer's patches in vivo, and it is proposed that this effect is mediated by T cell-VIP interactions in the vicinity of the specialized endothelium of those tissues.

scholarly journals Eosinophilia in transgenic mice expressing interleukin 5.

1990 ◽  
Vol 172 (5) ◽  
pp. 1425-1431 ◽  
Author(s):  
L A Dent ◽  
M Strath ◽  
A L Mellor ◽  
C J Sanderson
Keyword(s):  
Bone Marrow ◽  
Transgenic Mice ◽  
Lymph Nodes ◽  
Peyer's Patches ◽  
Peyer’S Patches ◽  
Mesenteric Lymph Nodes ◽  
Gene Encoding ◽  
Interleukin 5

Experiments in vitro suggest that although interleukin 5 (IL-5) stimulates the late stages of eosinophil differentiation, other cytokines are required for the generation of eosinophil progenitor cells. In this study transgenic mice constitutively expressing the IL-5 gene were established using a genomic fragment of the IL-5 gene coupled to the dominant control region from the gene encoding human CD2. Four independent eosinophilic transgenic lines have thus far been established, two of which with 8 and 49 transgene copies, are described in detail. These mice appeared macroscopically normal apart from splenomegaly. Eosinophils were at least 65- and 265-fold higher in blood from transgenics, relative to normal littermates, and approximately two- or sevenfold more numerous relative to blood from mice infected with the helminth Mesocestoides corti. Much more modest increases in blood neutrophil, lymphocyte, and monocyte numbers were noted in transgenics, relative to normal littermates (less than threefold). Thus IL-5 in vivo is relatively specific for the eosinophil lineage. Large numbers of eosinophils were present in spleen, bone marrow, and peritoneal exudate, and were highest in the line with the greatest transgene copy number. Eosinophilia was also noted in histological sections of transgenic lungs, Peyer's patches, mesenteric lymph nodes, and gut lamina propria but not in other tissues examined. IL-5 was detected in the sera of transgenics at levels comparable to those seen in sera from parasite-infected animals. IL-3 and granulocyte/macrophage colony-stimulating factor (GM-CSF) were not found. IL-5 mRNA was detected in transgenic thymus, Peyer's patches, and superficial lymph nodes, but not in heart, liver, brain, or skeletal muscle or in any tissues from nontransgenics. Bone marrow from transgenic mice was rich in IL-5-dependent eosinophil precursors. These data indicate that induction of the IL-5 gene is sufficient for production of eosinophilia, and that IL-5 can induce the full pathway of eosinophil differentiation. IL-5 may therefore not be restricted in action to the later stages of eosinophil differentiation, as suggested by earlier in vitro studies.

Vasoactive intestinal peptide modulates T lymphocyte migration in Peyer's patches of rat small intestine

1997 ◽  
Vol 272 (1) ◽  
pp. G92-G99 ◽  
Author(s):  
S. Miura ◽  
H. Serizawa ◽  
Y. Tsuzuki ◽  
I. Kurose ◽  
M. Suematsu ◽  
...  
Keyword(s):  
Vasoactive Intestinal Peptide ◽  
T Lymphocyte ◽  
Inhibitory Effect ◽  
Peyer's Patches ◽  
Peyer’S Patches ◽  
Intracellular Camp ◽  
Cell Trafficking ◽  
Lymphocyte Migration

Although vasoactive intestinal peptide (VIP) has been postulated to function in modulation of T cell trafficking, the exact mechanism has not been elucidated in vivo. In the present study, the effects of VIP on T lymphocyte migration were examined in rat Peyer's patches. T lymphocytes collected from intestinal lymph of rats were labeled with carboxyfluorescein diacetate succinimidyl ester and injected into the jugular vein. Peyer's patches of the recipient rats were observed with intravital fluorescence microscopy. In vivo intra-arterial infusion of or in vitro incubation with VIP did not affect the initial lymphocyte interaction with postcapillary venules of Peyer's patches. However, these treatments with VIP significantly inhibited transendothelial migration and also significantly blocked the interstitial migration of T cells and inhibited their subsequent appearance in the interfollicular lymphatics. Treatment with adenosine 3',5'-cyclic monophosphate (cAMP)-inducing agents resulted in similar inhibitory effect on T lymphocyte migration in Peyer's patches. In conclusion, VIP has significant inhibitory effects on T lymphocyte migration in Peyer's patches, possibly mediated by elevation of the intracellular cAMP concentrations.

scholarly journals Commensal microbiota drive proliferation of conventional and Foxp3+Regulatory CD4+T cells in mesenteric lymph nodes and Peyer's patches

2013 ◽  
Vol 3 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Sascha Cording ◽  
Diana Fleissner ◽  
Markus M. Heimesaat ◽  
Stefan Bereswill ◽  
Christoph Loddenkemper ◽  
...  
Keyword(s):  
T Cells ◽  
Lymph Nodes ◽  
Cd4 T Cells ◽  
Peyer's Patches ◽  
Peyer’S Patches ◽  
Mesenteric Lymph Nodes ◽  
Commensal Microbiota ◽  
Mesenteric Lymph

scholarly journals Association of Lactobacillus spp. with Peyer's Patches in Mice

2001 ◽  
Vol 8 (2) ◽  
pp. 320-324 ◽  
Author(s):  
Laura Plant ◽  
Patricia Conway
Keyword(s):  
Peyer's Patches ◽  
Peyer’S Patches ◽  
Adhesion Assay ◽  
Scanning Electron Micrographs ◽  
Intestinal Tissue ◽  
High Adhesion ◽  
Preferential Binding ◽  
Scanning Electron

ABSTRACT Sixteen strains of Lactobacillus isolated from humans, mice, and food products were screened for their capacity to associate with Peyer's patches in mice. In preliminary experiments, in vitro binding to tissue pieces was assessed by scanning electron microscopy, and it was demonstrated qualitatively that 5 of the 16 strains showed some affinity for the Peyer's patches, irrespective of their association with the nonlymphoid intestinal tissue. Lactobacillus fermentum KLD was selected for further study, since, in addition to its intrinsically high adhesion rate, this organism was found to exhibit a preferential binding to the follicle-associated epithelium of the Peyer's patches compared with its level of binding to the mucus-secreting regions of the small intestine. Quantitative assessment of scanning electron micrographs of tissue sections which had been incubated with L. fermentum KLD or a nonbinding control strain, Lactobacillus delbruckii subsp.bulgaricus, supported these observations, since a marked difference in adhesion was noted (P < 0.05). This preferential association of strain KLD with the Peyer's patches was also confirmed with radiolabeled lactobacilli incubated with intestinal tissue in the in vitro adhesion assay. Direct recovery of L. fermentum KLD from washed tissue following oral dosing of mice revealed a distinct association (P < 0.05) between this organism and the Peyer's patch tissue. In contrast, L. delbruckii subsp. bulgaricus showed negligible binding to both tissue types in both in vitro and in vivo adhesion assays. It was concluded that L. fermentum KLD bound preferentially to Peyer's patches of BALB/c mice.

scholarly journals Enhancement of in vitro and in vivo antigen-specific antibody responses by interleukin 11.

1992 ◽  
Vol 175 (1) ◽  
pp. 211-216 ◽  
Author(s):  
T G Yin ◽  
P Schendel ◽  
Y C Yang
Keyword(s):  
T Cells ◽  
Antibody Titer ◽  
Specific Antibody ◽  
Antibody Responses ◽  
Rabbit Serum ◽  
Dependent Manner ◽  
Dose Dependent ◽  
Interleukin 11

The availability of large quantities of highly purified recombinant interleukin 11 (rhuIL-11) has allowed us to investigate the effects of rhuIL-11 on sheep red blood cell (SRBC)-specific antibody responses in the murine system. The results showed that rhuIL-11 was effective in enhancing the generation of mouse spleen SRBC-specific plaque-forming cells (PFC) in the in vitro cell culture system in a dose-dependent manner. These effects of rhuIL-11 were abrogated completely by the addition of anti-rhuIL-11 antibody, but not by the addition of preimmunized rabbit serum. Cell-depletion studies revealed that L3T4 (CD4)+ T cells, but not Lyt-2 (CD8)+ T cells, are required in the rhuIL-11-stimulated augmentation of SRBC-specific antibody responses. The effects of rhuIL-11 on the SRBC-specific antibody responses in vivo were also examined. RhuIL-11 administration to normal C3H/HeJ mice resulted in a dose-dependent increase in the number of spleen SRBC-specific PFC as well as serum SRBC-specific antibody titer in both the primary and secondary immune responses. In mice immunosuppressed by cyclophosphamide treatment, rhuIL-11 administration significantly augmented the number of spleen SRBC-specific PFC as well as serum SRBC-specific antibody titer when compared with the cyclophosphamide-treated mice without IL-11 treatment. These results demonstrated that IL-11 is a novel cytokine involved in modulating antigen-specific antibody responses in vitro as well as in vivo.

scholarly journals The Immune Regulatory Function of Lymphoproliferative Double Negative T Cells In Vitro and In Vivo

2002 ◽  
Vol 196 (2) ◽  
pp. 261-267 ◽  
Author(s):  
Megan S. Ford ◽  
Kevin J. Young ◽  
Zhuxu Zhang ◽  
Pamela S. Ohashi ◽  
Li Zhang
Keyword(s):  
T Cells ◽  
Fas Ligand ◽  
Lymphoproliferative Disease ◽  
Receptor Expression ◽  
Third Party ◽  
Regulatory Function ◽  
Double Negative ◽  
Double Negative T Cells

Lymphoproliferative (lpr) mice, which lack functional Fas receptor expression and develop autoimmune lymphoproliferative disease, have an accumulation of T cell receptor-αβ+CD4−CD8− (double negative T cells [DNTC]) in the periphery. The function of the accumulating DNTC is not clear. In this study we demonstrate that B6/lpr DNTC can dose dependently kill syngeneic CD8+ and CD4+ T cells from wild-type B6 mice through Fas/Fas ligand interactions in vitro. We also demonstrate that B6/lpr DNTC that are activated and expand in vivo are able to specifically down-regulate allogeneic immune responses mediated by syngeneic Fas+CD4+ and CD8+ T cells in vivo. B6/lpr DNTC that have been preactivated in vivo by infusion of either class I– (bm1) or class II– (bm12) mismatched allogeneic lymphocytes are able to specifically enhance the survival of bm1 or bm12, but not third-party skin allografts when adoptively transferred into naive B6+/+ mice. These findings clearly demonstrate that B6/lpr DNTC have a potent immune regulatory function in vitro and in vivo. They also provide new insights into the mechanisms involved in the development of autoimmune disease in lpr mice.

scholarly journals Stromal mesenteric lymph node cells are essential for the generation of gut-homing T cells in vivo

2008 ◽  
Vol 205 (11) ◽  
pp. 2483-2490 ◽  
Author(s):  
Swantje I. Hammerschmidt ◽  
Manuela Ahrendt ◽  
Ulrike Bode ◽  
Benjamin Wahl ◽  
Elisabeth Kremmer ◽  
...  
Keyword(s):  
T Cells ◽  
Stromal Cell ◽  
Tissue Tropism ◽  
Mesenteric Lymph Nodes ◽  
Activated T Cells ◽  
Mesenteric Lymph ◽  
In Vitro Activation ◽  
Lymph Node Cells

T cells primed in the gut-draining mesenteric lymph nodes (mLN) are imprinted to express α4β7-integrin and chemokine receptor CCR9, thereby enabling lymphocytes to migrate to the small intestine. In vitro activation by intestinal dendritic cells (DC) or addition of retinoic acid (RA) is sufficient to instruct expression of these gut-homing molecules. We report that in vivo stroma cells, but not DC, allow the mLN to induce the generation of gut tropism. Peripheral LN (pLN) transplanted into the gut mesenteries fail to support the generation of gut-homing T cells, even though gut-derived DC enter the transplants and prime T cells. DC that fail to induce α4β7-integrin and CCR9 in vitro readily induce these factors in vivo upon injection into mLN afferent lymphatics. Moreover, uniquely mesenteric but not pLN stroma cells express high levels of RA-producing enzymes and support induction of CCR9 on activated T cells in vitro. These results demonstrate a hitherto unrecognized contribution of stromal cell delivered signals, including RA, on the imprinting of tissue tropism in vivo.

T Cell Trafficking in Acute GVHD: In Vivo Bioluminescence Evaluation To Elucidate the Role of Different Lymphatic Organs.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 593-593
Author(s):  
Andreas Beilhack ◽  
Stephan Schulz ◽  
Jeanette Baker ◽  
Georg F. Beilhack ◽  
Courtney B. Wieland ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Lymphoid Organs ◽  
The Body ◽  
Peyer's Patches ◽  
Peyer’S Patches ◽  
Alloreactive T Cells ◽  
Donor T Cells ◽  
Specific Priming

Abstract To study the complex pathophysiology of aGvHD in allogeneic hematopoietic cell transplantation (HCT) we transplanted transgenic luciferase expressing T cell populations into lethally irradiated HCT recipients (murine MHC major mismatch model, H-2q into H-2d). Tracking of light emitting donor T cells in living animals and detailed studies by multi color immunofluorescence microscopy (IFM) and FACS revealed the tight links of spatial and temporal evolution in this complex immune process. Donor derived T cells migrate to T cell areas in lymphoid tissues within a period of 12 hours. In the initial periods donor CD4+ T cells appear first with CD8+ T cell infiltration at later time points. Donor T cells start proliferating in lymphatic tissues on day 2 after transfer, as observed by BrdU stainings. Although alloreactive T cells are similarly activated in all lymphoid organs, they only up-regulate gut homing molecules after more than 5 cell divisions (CFSE proliferation analysis by FACS) in certain lymphoid organs (Peyer’s patches, mesenteric LN and spleen). Abruptly on day 4 after HCT, T cells migrate into intestinal sites. These findings strongly suggested, that specific priming sites are required for alloreactive T cells to induce a distinct type of tissue tropism in GvHD. In contrast to previous reports peformed without host conditioning, depletion of certain lymphoid organs (e.g. Peyer’s patches) before HCT or antibody blocking experiments did not control aGVHD. BLI showed, that anti-L-selectin or anti-MAdCAM-1 antibody treatment alone or in combination was effective in blocking donor T cell migration to lymph nodes and Peyer’s patches, while redirecting these cells to liver and spleen. Subsequently cells proliferated predominantly in the spleen until day 3 after HCT. Surprisingly we observed a full picture of gut infiltration on day 4 and skin involvement on day 5–6, similar in dynamics and strength to the aGvHD isotype control group. These findings demonstrated, that other lymphoid organs can functionally compensate for inducing gut and skin homing of alloreactive T cells. Of importance, we demonstrated that T cells that lacked homing molecules for secondary lymphoid organs had alloreactive properties in vitro, yet did not cause aGVHD in vivo. In summary, the activation of alloreactive T cells in specific sites throughout the body is complex and involves the acquisition of homing molecule expression. Transplantation of T cells with defined homing properties therefore, appears to be a promising alternative in conferring protective immunity early after HCT without the risk of aGvHD.

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