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At least 505 records · Page 28Linked to original sources
PubMed2002

CpG-oligodinucleotides as an effective adjuvant in pigs for intramuscular immunizations.

In this study, the effect of two oligodeoxynucleotide (ODN) sequences 5'GCT-AGA-CGT-TAG-CGT-3' (CpG-ODN) and 5'-GCT-AGA-GCT-TAG-GCT-3' (GpC-ODN) on the antigen-specific antibody and cellular immune response after intramuscular immunizations with OVA was analyzed in pigs. Pigs immunized with OVA supplemented with these ODNs showed a significantly enhanced primary antibody response in comparison with the control group which received OVA without ODN. This enhanced primary antibody response appeared ODN-sequence-independent as similar effects were seen in both ODN-groups. The OVA-specific antibody titers obtained after a single injection of antigen combined with either of both ODNs were as high as the titers in the control group after two injections. Furthermore, the ODN-supplemented animals showed significantly higher OVA-specific IgA antibodies in their saliva and nasal secretions at some time points after the first immunization. Proliferation assays showed that CpG- as well as GpC-ODN significantly enhanced the antigen-specific as well as the mitogen-induced proliferation in different lymphoid tissues. Furthermore, 48h after the third immunization the CpG-group showed a significantly decreased IL-6 mRNA expression in cells of the local draining lymph node but no significant difference in TGF-beta (Th3-like) and IL-10 (Th2-like). The ODN injected animals showed the tendency to have higher IFN-gamma (Th1-like) mRNA-expression in comparison with the control group. To our knowledge, these are the first in vivo studies in pigs, which demonstrate the appropriateness of CpG-ODN as immunostimulating adjuvants in vaccines for farm animals.

Adjuvants, Immunologic↗
PubMed1994

[Gnathostomiasis after a stay in Thailand].

During a 4-week holiday in Thailand a 13-year-old boy from Germany briefly fell ill with diarrhoea without blood-tinged stools and fever. 5 months later oedematous, reddish swellings occurred, at first on the right upper arm, later over the right side of the chest. Especially at night these swellings were associated with severe local and generalized itching. Bilaterally the axillary lymph-nodes were hard and slightly enlarged. There was a marked eosinophilia of 56%, the white count was 22,700/microliters and the serum level of IgE was raised to 1777 IU/ml. No worm eggs or larvae were found in the stool. Enzyme-linked immunosorbent assay, using larvae of Gnathostoma spinigerum as antigen, demonstrated antibodies against this nematode. Gnathostomiasis having been diagnosed treatment was started with albendazole (200 mg twice daily for 21 days), after which the boy was symptom free. After 2 months the eosinophilia had regressed to 10%, the white cell count was normal and the antibody titre had fallen.

Adolescent↗
PubMed2003

A blocking antibody to the hyaluronan receptor for endocytosis (HARE) inhibits hyaluronan clearance by perfused liver.

Hyaluronan (HA) and chondroitin sulfate clearance from lymph and blood is mediated by the hyaluronan receptor for endocytosis (HARE). The purification and molecular cloning (Zhou, B., Weigel, J. A., Saxena, A., and Weigel, P. H. (2002) Mol. Biol. Cell 13, 2853-2868) of this cell surface receptor were finally achieved after we developed monoclonal antibodies (mAbs) against HARE. There are actually two independent isoreceptors for HA, which in rat are designated the 175-kDa HARE and 300-kDa HARE. Only one mAb (number 174) effectively and completely blocked the specific uptake of 125I-HA at 37 degrees C by rat liver sinusoidal endothelial cells. 125I-HA binding to both the 175-kDa and 300-kDa HARE proteins in a ligand blot assay was almost completely inhibited by <1 microg/ml mAb-174, whereas mouse IgG had little or no effect. MAb-174 also performed very well in Western analysis, indirect fluorescence microscopy, and a variety of immuno-procedures. Immunohistochemistry using mAb-174 localized HARE to the sinusoidal cells of rat liver, spleen, and lymph node. Western analysis using mAb-174 revealed that the sizes of both HARE glycoproteins were the same in these three tissues. 125I-HA was taken up and degraded by excised rat livers that were continuously perfused ex vivo with a recirculating medium. This HA clearance and metabolism by liver, which is a physiological function of HARE, was very effectively blocked by mAb-174 but not by mouse IgG. The results indicate that mAb-174 will be a useful tool to study the functions of HARE and the physiological significance of HA clearance.

Animals↗
PubMed1990

A bovine monoclonal antibody detecting a class I BoLA antigen.

The bovine IgG1 monoclonal antibody (mAb) ILA70 was made by immunizing a calf with peripheral blood mononuclear cells (PBM) from a BoLA-w10 homozygous heifer and subsequently fusing lymphocytes from the local lymph-node with the heterohybridoma 53B3. Family and population studies, antibody binding inhibition and immunoprecipitation of the target antigen all indicate that ILA70 detects a polymorphic epitope on a bovine class I major histocompatibility complex (MHC) molecule. The antibody is complement fixing and so may be used in a standard cytotoxicity assay. Ascitic fluid with antibody activity many times greater than that of the tissue-culture supernatant has been prepared in nude mice. The antibody-producing heterohybridoma has been subcloned three times and appears to be stable. Such heterohybridomas may prove to be a valuable source of particularly discriminating and informative mAbs for the serological analysis of the products of the bovine MHC.

Animals↗
PubMed1989

Function and regulation of the neutrophil MEL-14 antigen in vivo: comparison with LFA-1 and MAC-1.

The CD11/18 (LFA-1, Mac-1) molecules participate in neutrophil adhesion to cultured endothelium in vitro and are critical for effective neutrophil localization into inflamed tissues in vivo. More recently, the MEL-14 Ag, which was first defined as a lymphocyte homing receptor, has also been implicated in inflammatory neutrophil extravasation. Here we compare the regulation and function of these adhesion molecules on neutrophils during the in vivo inflammatory response. The MEL-14 Ag is expressed at high levels on bone marrow and peripheral blood neutrophils, but is lost on neutrophils isolated from the thioglycollate-inflamed peritoneal cavity. In contrast, Mac-1 is up-regulated on inflammatory neutrophils and little change is seen in the level of LFA-1 expression. In vitro activation of bone marrow neutrophils with PMA or leukotriene B4 results in a dose dependent increase in Mac-1 and decrease in MEL-14 Ag expression within 1 h after treatment, thus reflecting what is found during inflammation in vivo. Neutrophils activated in vitro or in vivo (MEL-14Low, Mac-1Hi) do not home to inflammatory sites in vivo, correlating with the loss of the MEL-14 Ag and the increased Mac-1 expression. Anti-LFA-1, anti-Mac-1, or MEL-14 antibody given i.v. suppress neutrophil accumulation within the inflamed peritoneum (38%, 30%, and 37% of medium control, respectively) without affecting the levels of circulating neutrophils. However, when FITC-labeled cells are precoated with the mAb and injected i.v., only MEL-14 inhibits extravasation into the inflamed peritoneum (25% of medium control). Finally, in ex vivo adhesion assays of neutrophil binding to high endothelial venules in inflamed-lymph node frozen sections MEL-14 inhibits greater than 90%. anti-LFA-1 20 to 30% and anti-Mac-1 less than 10% of the binding of bone marrow neutrophils to inflamed-lymph node high endothelial venules. These results confirm that both the MEL-14 antigen and Mac-1/LFA-1 are important in neutrophil localization to inflamed sites in vivo, but suggest that their roles in endothelial cell interactions are distinct.

Animals↗
PubMed1983

Germinal center B cells lack homing receptors necessary for normal lymphocyte recirculation.

Germinal center B cells (GCLC) are a discrete population of antigen-activated lymphoblasts that lack surface IgD and express abundant cell surface binding sites for peanut agglutinin (PNA). These phenotypic features render GCLC easily distinguishable from nearly all plasma cells, T cells, and unstimulated B cells, and have enabled us to identify and isolate GCLC from antigen-stimulated murine lymphoid organs. We have examined the migratory properties of these lymphoblasts in (a) short-term in vivo homing studies, and (b) an in vitro assay of lymphocyte binding to post-capillary, high endothelial venules (HEV) in frozen sections of Peyer's patches and peripheral lymph nodes. In the in vivo experiments, intravenously injected GCLC failed to migrate in significant numbers to peripheral lymphoid organs in comparison with T cells or IgD+ B cells. In the in vitro binding assay, GCLC did not adhere to HEV in either Peyer's patch or peripheral node sections. A variety of factors, such as preferential sequestration in the liver, may operate in vivo to influence the localization of these cells. However, their nearly total failure to migrate into lymphoid organs can best be explained by their inability to recognize and adhere to the specialized HEV which normally mediate the emigration of recirculating lymphocytes from the blood into these sites. The concept that GCLC fail to express functional homing receptors for HEV has been further supported by studies using MEL-14, a monoclonal antibody that appears to recognize the lymphocyte surface receptor for peripheral node HEV: In contrast to most peripheral lymphocytes, GCLC fail to bind MEL-14. These migratory and endothelial-recognition properties of GCLC, when viewed in the context of the possible role of these cells as precursors of plasma cells and/or memory B cells, have led us to propose that the inability of GCLC to recognize HEV may be transient and related to a phase of sessile B cell differentiation.

Animals↗
PubMed2002

Progression of armed CTL from draining lymph node to spleen shortly after localized infection with herpes simplex virus 1.

We have examined the generation of CTL immunity immediately after localized footpad infection with herpes simplex virus 1 (HSV-1) using three coordinated in vivo T cell tracking methodologies. Tetrameric MHC class I containing the immunodominant peptide from HSV-1 glycoprotein B (gB) showed that after infection the proportion of Ag-specific T cells peaked at day 5 within draining popliteal lymph nodes and 2 days later in the spleen. Preferential expression of the activation marker CD25 by tetramer-positive cells in draining popliteal nodes but not spleen suggested that gB-specific T cells were initially activated within the lymph node. In vivo cytotoxicity assays showed that Ag-specific effector cells were present within the draining lymph nodes as early as day 2 after infection, with a further 2-day lag before detection in the spleen. Consistent with the very early arming of effector CTL in the draining lymph node, adoptive transfer of CFSE-labeled gB-specific transgenic T cells showed that they had undergone one to four rounds of cell division by day 2 after infection. In contrast, proliferating T cells were first detected in appreciable numbers in the spleen on day 4, at which time they had undergone extensive cell division. These data demonstrate that HSV-1-specific T cells are rapidly activated and armed within draining lymph nodes shortly after localized HSV-1 infection. This is followed by their dissemination to other compartments such as the spleen, where they further proliferate in an Ag-independent fashion.

Animals↗
PubMed2004

Intratumoral IL-12 and TNF-alpha-loaded microspheres lead to regression of breast cancer and systemic antitumor immunity.

BACKGROUND: Local, sustained delivery of cytokines at a tumor can enhance induction of antitumor immunity and may be a feasible neoadjuvant immunotherapy for breast cancer. We evaluated the ability of intratumoral poly-lactic-acid-encapsulated microspheres (PLAM) containing interleukin 12 (IL-12), tumor necrosis factor alpha (TNF-alpha), and granulocyte-macrophage colony stimulating factor (GM-CSF) in a murine model of breast cancer to generate a specific antitumor response. METHODS: BALB/c mice with established MT-901 tumors underwent resection or treatment with a single intratumoral injection of PLAM containing IL-12, TNF-alpha, or GM-CSF, alone or in combination. Two weeks later, lymph nodes and spleens were harvested, activated with anti-CD3 monoclonal antibodies (mAb) and rhIL-2, and assessed for antitumor reactivity by an interferon gamma (IFNgamma) release assay. Tumor-infiltrating lymphocyte (TIL) analysis was performed on days 2 and 5 after treatment by mechanically processing the tumors to create a single cell suspension, followed by three-color fluorescence-activated cell sorter (FACS) analysis. RESULTS: Intratumoral injection of cytokine-loaded PLAM significantly suppressed tumor growth, with the combination of IL-12 and TNF-alpha leading to increased infiltration by polymorphonuclear cells and CD8+ T-cells in comparison with controls. The induction of tumor-specific reactive T-cells in the nodes and spleens, as measured by IFN-gamma production, was highest with IL-12 and TNF-alpha. This treatment resulted in resistance to tumor rechallenge. CONCLUSIONS: A single intratumoral injection of IL-12 and TNF-alpha-loaded PLAM into a breast tumor leads to infiltration by polymorphonuclear cells and CD8+ T-cells with subsequent tumor regression. In addition, this local therapy induces specific antitumor T-cells in the lymph nodes and spleens, resulting in memory immune response.

Animals↗
PubMed1975

Inhibition of the graft-versus-host reaction. III. Altered in vivo distribution of spleen cells pretreated with Fab fragments of antithymocyte globulin.

51Cr-labeled parental strain spleen cells were pretreated in vitro with antithymocyte globulin (ATG) or Fab fragments of ATG before i.v. injection into F1 recipients. Recipients were killed at various intervals after injection and their organs were assayed for radioactivity in order to determine the in vivo distribution pattern of pretreated cells. 51Cr spleen cells pretreated with ATG were almost totally prevented from migrating to spleens, lymph nodes, bone marrow, Peyer's patches, lungs, and peripheral blood of recipients. Pretreatment of 51Cr spleen cells with noncytotoxic Fab of ATG also inhibited localization to these organs and tissues; however, the inhibition was not as complete as that of ATG-treated cells. Localization of Fab-treated 51Cr spleen cells to recipient nodes was inhibited to a greater extent than was localization to recipient spleens. There was no significant difference in the extent of inhibition of ATG-treated 51Cr spleen cells to recipient nodes and spleen. Organ counts from recipients killed at various intervals after injection of Fab-treated 51Cr spleen cells showed that Fab-treated cells do not recover their recirculating potential in vivo.

Animals↗
PubMed2002

Immunotherapy with recombinant SFV-replicons expressing the P815A tumor antigen or IL-12 induces tumor regression.

Replicons based on alphaviruses are emerging as candidate vectors for vaccination and gene therapy purposes. We have reported previously that mice vaccinated with a recombinant Semliki Forest virus (a member of the alphavirus genus) carrying the gene encoding the P815A tumor antigen (rSFV/E-P1A) were protected against a lethal challenge with the P815 tumor. In this study we investigated the anti-tumor therapeutic efficacy of rSFV/E-P1A or rSFV expressing the cytokine interleukin 12 (rSFV/IL12) on Day 5-established tumors. The results show that both antigen-specific and cytokine-mediated rSFV treatments exhibited a significant effect on P815 tumor growth, by delaying tumor progression and even inducing complete tumor regressions in several mice. The therapeutic potency of these vectors was dependent on the size of the treated tumor, as treatment of mice bearing larger tumors showed lower efficacy. In addition, rSFV treatment resulted in long-term immunity as observed by the lack of tumor recurrence in the majority of tumor-regressing mice after rechallenge with the tumor. Furthermore, the anti-tumor therapeutic effect was only achieved by local intratumoral injection of rSFV, as treatment by injection in the contralateral site resulted in tumor progression comparable to control-untreated mice. Accordingly, expression of a rSFV-RNA was localized to the tumor and draining lymph node. These results further demonstrate the potential of rSFV replicons as tumor therapeutic agents.

Animals↗
PubMed2002

Localisation of CD25+ cells and MHCII+ cells in lymph nodes draining Mycobacterium avium subsp. paratuberculosis vaccination granuloma and the presence of a systemic immune response.

Vaccination of goat kids against paratuberculosis protects against lesions and clinical disease. The systemic cellular response was studied in goat kids 3-9 weeks after vaccination. Peripheral blood cells showed increased interferon-gamma production and expression of interleukin-2 receptor (CD25) after stimulation with Mycobacterium avium subsp. paratuberculosis antigens. The lymph node draining the vaccination granuloma was studied three weeks after vaccination in a parallel group of goat kids. In deep cortex, MHCII+ cells were observed surrounded by CD4+ T-cells, while follicular hypertrophy and hyperplasia were prominent in the subcapsular region and along connective tissue trabecula. Comparison of the local and systemic immune responses revealed an inverse relationship between CD25+ T-cells in the lymph node deep cortex and cells in peripheral blood that up-regulate CD25 upon in vitro stimulation, suggesting that activated and regulatory T-cells in the local lymph node influence the level of circulating antigen-specific T-cells following vaccination against paratuberculosis in goats.

Animals↗
PubMedDate not supplied

Does local hyperthermia affect metastasis of a human prostate carcinoma grown in athymic nude mice?

PRIMARY OBJECTIVE: This study investigated whether local hyperthermia increases metastasis of prostate carcinoma xenografts in athymic nude mice. RESEARCH DESIGN AND METHODS: Human prostate carcinoma cells (1-LN-PC-3-1A) were injected into the animal's thigh. Mice were randomly divided into those treated with local hyperthermia (43 degrees C for 45 min, tumour volume 100 or 200 mm(3)) and untreated controls, and sacrificed when the tumour volume reached 500 mm(3). MAIN OUTCOMES AND RESULTS: Histological evaluation (hematoxylin and eosin staining) of lymph nodes showed metastases in 20/21 hyperthermia-treated and 17/21 control mice. Lymph node involvement, tumour weight at sacrifice, and tumour growth rate were not significantly different between groups. CONCLUSION: Single local hyperthermia treatment had no effect on lymph node metastatic spread in this model.

Animals↗
PubMed1994

[High endothelial venule and lymphocyte homing of the musk shrew palatine tonsil].

Homing of lymphocytes into secondary lymphoid organs is essential for an adequate immune response in vivo. Adherence of the lymphocytes to the high endothelial venule (HEV) is the crucial step of the homing. In contrast to lymph nodes and Peyer's patch, study of lymphocyte homing to the palatine tonsil has been hampered by the lack of useful laboratory animals that possess the tonsil. Herein, we examined the preferential adhesion of lymphocytes to the tonsillar HEV using the musk shrew; a new laboratory animal which has a pair of immunocompetent palatine tonsils. The palatine tonsils of the musk shrew had the morphologically detectable HEV in the parafollicular region. Immunofluorescent staining showed that more B cells were located in the lumen of the tonsillar HEV rather than T cells. The in vitro lymphocyte-HEV binding assay indicated some preferential adhesion of the lymphocytes to the tonsillar HEV. First, adhesion of B cells to the tonsillar HEV was more preferential than that of T cells, which was consistent with the result in the assay of Peyer's patch. Second, adhesion of the lymphocytes from axillar and inguinal lymph nodes was similar to that of the lymphocytes from the mesenteric lymph nodes, that differed from the result in the assay of Peyer's patch. These findings suggest that, in the musk shrew, the regulation of lymphocyte homing through the HEV has differences between tonsil and Peyer's patch, at least in part. This may be related to the role of the lymphoid organs in each local immune response.

Animals↗
PubMed1984

Immunologic dysfunction during viral oncogenesis. II. Inhibition of cellular immunity to viral antigens by malignant rabbit fibroma virus.

The ability of two related viruses--Shope fibroma virus (SFV) and malignant rabbit fibroma virus (MV)--to induce virus-specific immune responses in lymphocytes of recipient animals was studied. SFV produces a benign local tumor which regresses in 12-14 days. Using an assay for virus-induced lymphocyte blastogenesis lymphocytes reactive to SFV were detected, both in rabbits bearing SFV-induced tumors and in rabbits whose SFV-induced tumor had regressed. These virus-reactive cells were detected in peripheral blood and spleen, and in lymph nodes draining the primary tumor. In contrast, MV produces a disseminated tumor and eventual death. MV does not induce detectable blastogenic responses in lymphocyte populations. SFV and MV are antigenically cross reactive: rabbits immune to SFV do not develop MV-induced tumors, and antisera to each virus neutralize both equally. Lymphocytes from SFV-infected rabbits proliferate in vitro in response to MV that has been inactivated by ultraviolet light (uv/MV) but not to infectious MV. In contrast, lymphocytes from rabbits infected with MV do not respond to uv-inactivated MV or to SFV. Thus, infectious MV inhibits the development of normal blastogenic responses in vivo and prevents the expression of those responses in lymphocytes from MV-resistant, SFV-immune rabbits in vitro. The relevance of this impairment to the differences in the clinical courses of SFV- and MV-induced tumors is discussed.

Animals↗
PubMed1995

Neonatal impaired response to viral superantigen encoded by MMTV(SW) and Mtv-7.

MMTV(SW) is an exogenous mouse mammary tumor virus that codes for a superantigen sharing the same V beta specificity as Mtv-7 (Mis-1a). Neonatal mice infected by suckling-infected milk show a deletion of the CD4+ V beta 6+ T cell subset within 8 weeks. In contrast, adult mice infected by injection of the virus in the footpad have a much faster deletion, which occurs within 2 weeks. In the present work, we investigated possible mechanisms for the different kinetics of deletion in the adult and newborn mice. To find out if the route of infection could be responsible for this discrepancy, we infected 5-day-old and adult mice by injection in the footpad. Our results demonstrate that the route of infection is not responsible for the delayed kinetics of reactive T cell deletion since newborn mice injected with the virus show similar kinetics to neonates infected by maternal milk. To exclude differences in viral spreading between the two models, we used a PCR assay to detect proviral DNA. Spreading of the virus was shown to occur at a similar rate or even more rapidly in neonates than in adults. We also compared the activation induced by MMTV(SW) or Mis-1a spleen cells in the draining lymph node in neonatal and adult mice and showed that a poor local activation is induced in neonates compared with adults. In vitro, neonatal T cell reactivity to anti-V beta 6 antibody was also impaired. Thus, the delay in clonal deletion could be linked to impaired expression, presentation and/or response to the viral superantigen. Our results suggest that the initial response to MMTV(SW) could be of importance for the kinetics of reactive T cell deletion.

Animals↗
PubMed1993

A primary intestinal helminthic infection rapidly induces a gut-associated elevation of Th2-associated cytokines and IL-3.

The immune response that is characteristic of parasitic helminth infections includes components associated with immediate-type hypersensitivity: elevated serum IgE, eosinophilia, and intestinal mast cell hyperplasia. In infection with the parasitic nematode, Heligmosomoides polygyrus, IL-4 mediates protective immunity, suggesting the presence of a host-protective Th2 response. In this investigation, we examined early stages of immune responsiveness to H. polygyrus infection to determine whether and at what stage a specific Th2-like pattern first appears. Using a quantitative reverse transcriptase-polymerase chain reaction assay, we analyzed changes in IL-2, IFN-gamma, IL-3, IL-4, IL-5, IL-6, IL-9, and IL-10 gene expression in the spleen, mesenteric lymph node, and Peyer's patch at various time points after infection. Our results demonstrate a highly specific and reproducible pattern of cytokine gene expression that remains localized to the enteric region. By 6 h after infection, IL-5 and IL-9 mRNA were elevated in the Peyer's patch and IL-3 was elevated by 12 to 24 h after infection. IL-4 RNA became elevated by 4 to 6 days after infection, but little change was observed in IFN-gamma, IL-2, or IL-10 mRNA levels. The early increases in IL-3, IL-5, and IL-9 gene expression after infection were probably T cell-independent, inasmuch as they were observed in Peyer's patches of congenitally athymic mice and anti-CD4, anti-CD8 mAb-treated conventional mice. However, treatment with these mAb considerably decreased cytokine gene expression 6 days after infection, and 8 days after infection, increased IL-4 gene expression in mesenteric lymph node cells was restricted to the CD4+ population. Thus, H. polygyrus infection induces cytokine gene expression that is restricted to some Th2-associated cytokines, is initiated by a T-independent response, and culminates in a T-dependent response.

Animals↗
PubMed1997

The migratory behavior of murine CD4+ cells of memory phenotype.

Lymphocyte differentiation is connected with profound alterations in the migratory pattern of lymphocytes. Whereas naive cells predominantly recirculate through lymphoid tissues, activated lymphocytes acquire an increased preference for immigration into non-lymphoid tissues and a reduced capacity for recirculation via high endothelial venules (HEV). A variety of data had indicated that memory-related subpopulations of cells in man and sheep, classified by the low expression of the CD45RA isotype, also lack the capacity to recirculate via HEV. However, recent data in the rat called these results into question. We therefore analyzed the migration properties of murine CD4+ T cell subpopulations defined by several markers used to distinguish memory from naive CD4+ cells in mice, namely CD45RB, L-selectin and CD44. Our data clearly show that the majority of putative memory cells expressing either low levels of CD45RB, low levels of L-selectin or high levels of CD44 display a strongly reduced capacity for direct entry into lymphoid tissues, including the spleen, from the blood stream. The accumulation in peripheral lymph nodes is further reduced by treatment with anti-L-selectin antibody, which blocks their entry via HEV. This indicates that memory CD4+ T cells are not excluded from crossing lymph node HEV, and that the numbers of cells entering the node via this route exceed the numbers entering via the afferent lymph, at least in the absence of local inflammation. Concomitantly, a strongly enhanced localization of cells of the memory phenotype is observed in lung and liver as compared with naive cells. Trafficking to specific sites such as skin or gut mucosa is not a prominent feature of the total population of memory cells. The trafficking to lung and liver and an increased ability to bind to dendritic cells, demonstrable in in vitro adhesion assays, suggest a more sessile phenotype of most memory cells. With respect to these properties, memory cells have a surprizing similarity to fully activated lymphocytes.

Animals↗