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Results for “Lymphocyte Transfusion”

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PubMed1974

Passive transfer of delayed-type hypersensitivity to cell walls of Staphylococcus aureus.

Protracted inflammatory dermal reactions to staphylococcal cell walls were observed in guinea pigs passively sensitized by transfer of peritoneal exudate cells but not by immune serum from guinea pigs actively sensitized with heat-killed cells of Staphylococcus aureus. The experiments verify the hypothesis that the protracted reaction is a cell-mediated immune response which is resolvable from the toxicity of the cell walls.

Animals↗
PubMed1993

Herpetic stromal keratitis in the reconstituted scid mouse model.

Infections of the cornea with herpes simplex virus type 1 cause inflammatory lesions which frequently lead to blindness. The disease is suspected to be immunopathological in nature. To establish this point and to study possible mechanisms involved, corneal infections in C.B-17 scid/scid and cell-reconstituted scid mice were investigated. Whereas unreconstituted scid mice failed to develop herpetic stromal keratitis (HSK) and died of encephalitis, mice reconstituted with T lymphocytes generated severe lesions. T cells of the CD4+ subset were found to be essential mediators of the HSK lesion, while T cells of the CD8+ subset protected mice from lethality. The results confirm that HSK is an immunopathological disease and that scid mice provide a convenient model that should prove valuable in establishing the biochemical mechanisms by which HSK is mediated.

Animals↗
PubMed2000

Relative sensitivity of hepatitis B virus and other hepatotropic viruses to the antiviral effects of cytokines.

We have previously shown that hepatitis B virus (HBV) replication is inhibited noncytopathically in the livers of transgenic mice following injection of HBV-specific cytotoxic T lymphocytes (CTLs) or infection with unrelated hepatotropic viruses, including lymphocytic choriomeningitis virus (LCMV) and adenovirus. These effects are mediated by gamma interferon (IFNgamma), tumor necrosis factor alpha (TNFalpha), and IFNalpha/beta. In the present study, we crossed HBV transgenic mice with mice genetically deficient for IFNgamma (IFNgammaKO), the TNFalpha receptor (TNFalphaRKO), or the IFNalpha/beta receptor (IFNalpha/betaRKO) in order to determine the relative contribution of each cytokine to the antiviral effects observed in each of these systems. Interestingly, we showed that HBV replicates in unmanipulated IFNgammaKO and IFNalpha/betaRKO mice at levels higher than those observed in control mice, implying that baseline levels of these cytokines control HBV replication in the absence of inflammation. We also showed that IFNgamma mediates most of the antiviral effect of the CTLs while IFNalpha/beta is primarily responsible for the early inhibitory effect of LCMV and adenovirus on HBV replication. In addition, we showed that the hepatic induction of IFNalpha/beta observed after injection of poly(I. C) is sufficient to inhibit HBV replication and that a similar antiviral effect is achieved by systemic administration of very high doses of IFNalpha. We also compared the relative sensitivity of LCMV and adenovirus to control by IFNgamma, TNFalpha, or IFNalpha/beta in these animals. Importantly, IFNalpha/betaRKO mice, and to a lesser extent IFNgammaKO mice, showed higher hepatic levels of LCMV RNA and adenovirus DNA and RNA than control mice, underscoring the importance of both interferons in controlling these other viral infections as well.

Adenoviridae↗
PubMed1978

Suppression of rejection of Nippostrongylus brasiliensis in iron and protein deficient rats: effect of syngeneic lymphocyte transfer.

Rejection of Nippostrongylus brasiliensis is impaired in iron and protein deficient rats and this suggests that iron and protein deficiency directly or indirectly suppresses the immune response. The site of the immunological defect in deficient rats was investigated using the technique of cellular transfer of resistance. The functional activity of immune mesenteric lymph node cells obtained from iron and protein deficient donors was not depressed as measured by their capacity to cause parasite rejection in nutritionally sufficient recipients. In contrast, immune lymph node cells obtained from either sufficient or deficient donors did not result in parasite rejection in iron and protein deficient recipients. These results indicate that there is no permanent defect of lymphocyte function in iron and protein deficient rats and suggest that either some other component of the rejection mechanism is defective, or that lymphocyte function is blocked in an iron and protein deficient environment.

Animals↗
PubMed1997

Induction of intestinal lesions in nu/nu mice induced by transfer of lymphocytes from syngeneic mice infected with murine retrovirus.

BACKGROUND: Murine leukemia virus, LP-BM5, induces severe immunodeficiency with abnormal lymphoproliferation in susceptible C57BL/6 mice. In a previous study, it was shown that a Sjögren's syndrome-like systemic exocrinopathy is induced in the virus infected mice. AIMS: To examine lymphocyte functions of the virus infected mice. METHODS: Four-week old mice were inoculated with the virus and their spleen cells were transferred into syngeneic nu/nu mice. Their organs were examined by light and electron microscopy. Phenotypes of the colon infiltrating cells were examined by flow cytometry. RESULTS: All nu/nu recipients had died by six weeks after cell transfer, showing runting disease like cachexia with diarrhoea and anal bleeding. Histopathological examination revealed that systemic exocrinopathy was adoptively transferable and that the colon became thickened due to mononuclear cell infiltration into the mucosal and submucosal layer with hyperplasia of intestinal epithelial cells. No virus particles were found in the colon. Flow cytometric analyses revealed that most of the infiltrating CD4+ T cells showed CD45RBlow. No intestinal lesions were observed in the virus infected mice nor in nu/nu mice inoculated with normal lymphocytes. CONCLUSION: Lymphocytes of the virus infected mice induced colitis and hyperplasia of intestinal epithelial cells as well as systemic exocrinopathy in nu/nu mice. Our experimental system may give some insight into intestinal lesions associated with virus infection.

Animals↗
PubMed1991

The SCID mouse mutant: definition, characterization, and potential uses.

Mice homozygous for the scid mutation (scid mice) are severely deficient in functional B and T lymphocytes. The mutation appears to impair the recombination of antigen receptor genes and thereby causes an arrest in the early development of B and T lineage-committed cells; other hematopoietic cell types appear to develop and function normally. The arrest in lymphocyte development is not absolute; some young adult scid mice are "leaky" and generate a few clones of functional B and T cells. By 10-14 months of age, virtually all scid mice are leaky. Scid mice readily support normal lymphocyte differentiation and can be reconstituted with normal lymphocytes from other mice and even partially reconstituted with human lymphocytes. They also support the growth of allogeneic and xenogeneic tumors. Thus, scid mice are of interest for studies of both normal and abnormal lymphocyte development and function. In addition, they can be used to study the function of nonlymphoid cell types in the absence of lymphocytes.

Animals↗
PubMed1985

Biodistribution of radiolabeled lymphocytes.

Factors that might affect the biodistribution and clinical utility of radiolabeled lymphocytes were evaluated in experimental animals. Indium-111 (In-111) labeled lymphocytes (10(7)-10(9) syngeneic or allogeneic cells; 1-10 microCi [.037-.37 MBq]/10(8) cells) obtained from peripheral blood, lymph node, or spleen were found in significant amounts in the lymphoid tissues of Lewis rats as early as 3 hours after infusion. A progressive increase in nodal activity with concomitant fall of activity in other organs followed, indicating active recirculation of the lymphocytes. However, In-111 labeled thymocytes or xenogeneic lymphocytes failed to accumulate in lymphoid tissue. In vitro irradiation of the In-111 labeled lymphocytes (100-400 rads [1-4 Gy]) before in vivo administration and increase of the In-111 to 40 microCi [1.48 MBq]/10(8) lymphocytes resulted in no detectable lymphocyte recirculation and/or reduced localization in lymphoid tissue. Splenectomized animals and those sensitized to an organ allograft before cell infusion showed increased activity in their bone marrow. These results suggest that the source of the injected cells, cell irradiation dose level, and host sensitization should be considered when radiolabeled lymphocytes are being prepared for use in clinical diagnosis and therapy.

Animals↗
PubMed1998

Lymphocyte transfer in streptozotocin-induced diabetes: adhesion of donor cells to islet endothelium.

The interaction between intravenously transferred lymphocytes derived from spleens of multiple low-dose streptozotocin-diabetic mice with islet, exocrine pancreatic, and gastric mucosal endothelium of nondiabetic recipient mice was investigated by in vivo microscopy. Donor lymphocytes were stained with acridine red in vitro. The adoptive transfer of these cells from diabetic donor animals resulted in significantly increased lymphocyte rolling (4.46 +/- 1.32%, P < 0.05) and adhesion (3.86 +/- 1.04%, P < 0.05) in islets of nondiabetic recipients that had been pretreated with a single subdiabetogenic dose of streptozotocin. No increased endothelial interaction was noted in nonpretreated recipients or in experiments with nondiabetic donors. Rolling (1.19 +/- 0.61 to 2.71 +/- 0.62%) and adhesion (0.61 +/- 0.33 to 2.80 +/- 0.97%) of donor lymphocytes were low in exocrine pancreatic and gastric mucosal control tissue. It is concluded that, in this animal model, lymphocytes from diabetic donors interact preferentially with recipient islet endothelium. However, additional stimulation of recipient islet endothelium by exogenous factors is necessary to enable transferred cells to adhere to pancreatic islets.

Animals↗
PubMed2005

Induction of early post-transplant graft-versus-leukemia effects using intentionally mismatched donor lymphocytes and elimination of alloantigen-primed donor lymphocytes for prevention of graft-versus-host disease.

Graft-versus-leukemia (GVL) effects can be induced in tolerant mixed chimeras prepared with nonmyeloablative conditioning. GVL effects can be amplified by post-grafting donor lymphocyte infusion (DLI). Unfortunately, DLI is frequently associated with graft-versus-host disease (GVHD). We investigated the feasibility of induction of potent GVL effects by DLI using intentionally mismatched lymphocytes followed by elimination of alloreactive donor T cells by cyclophosphamide for prevention of lethal GVHD following induction of very short yet most potent GVL effects. Mice inoculated with B-cell leukemia (BCL1) and mismatched donor lymphocytes were treated 2 weeks later with low-dose or high-dose cyclophosphamide. All mice receiving cyclophosphamide 2 weeks after DLI survived GVHD, and no residual disease was detected by PCR; all control mice receiving DLI alone died of GVHD. Analysis of host (female) and donor (male) DNA showed that cyclophosphamide treatment eradicated most alloreactive donor cells, yet mixed chimerism was converted to full donor chimerism following transient self-limited GVHD. Our working hypothesis suggests that short-term yet effective and safe adoptive immunotherapy of leukemia may be accomplished early post-transplantation using alloreactive donor lymphocytes, with prevention of GVHD by elimination of GVL effector cells.

Animals↗
PubMed2005

Renal cancer treatment with low levels of mixed chimerism induced by nonmyeloablative regimen using cyclophosphamide in mice.

Recently, much attention has been paid to nonmyeloablative allogeneic stem cell transplantation for the treatment of metastatic renal cancer. Mature donor T cells cause graft-versus-host disease (GVHD) although they are also the main mediators of the beneficial graft-versus-tumor activity associated with this treatment. Hence, the segregation of the graft-versus-tumor activity from GVHD is an important challenge in managing the clinical course of treatment. We previously reported a series of studies regarding the allograft tolerance induced by allogeneic spleen cells (with bone marrow cells) and cyclophosphamide in mice. Here, we show a modified cyclophosphamide-induced tolerance system for the treatment of murine renal cell carcinoma, RENCA, by shifting the equal balance between graft-versus-host and host-versus-graft reactions toward graft-versus-host reaction with donor lymphocyte infusion. Our results clearly show the antitumor activity against RENCA with only low levels of mixed chimerism in the periphery and the in vivo and in vitro acquired immunity against RENCA even when mixed chimerism is almost undetectable. Because the withdrawal of mixed chimerism reduces the risk of GVHD, the antitumor activity is thus sequentially segregated from the initial GVHD in our model. We believe that this is the first unique model system of nonmyeloablative allogeneic hemopoietic cell transplantation to ever be reported for the treatment of renal cancer.

Animals↗
PubMed2000

Hepatic lymphocyte transplantation in hyperbilirubinemic gunn rats.

Hepatic lymphomyeloid cells (HLCs) are thought to contain liver stem cells. We investigated whether HLCs generated enzyme-producing cells in vivo. HLCs from normal Wistar/Shi rats and rats in which liver ischemia was induced using a portal clamp 4 days previously were studied histopathologically and characterized using flow cytometry. Splenic lymphocytes obtained from these animals were compared as a control. The proliferative activity of HLCs and splenic cells from both groups was also tested by stimulation with concanavalin A. HLCs contained a significantly higher number of NK-T cells and OV6+ cells compared with the splenic cells. The HLCs from rats in which liver ischemia was induced tended to have greater proliferative activity than those from normal rats, while the proliferative activity of splenic lymphocytes was impaired by liver ischemia. The HLCs obtained from Wistar/Shi rats with liver ischemia were then injected into hereditary hyperbilirubinemic Gunn rats to determine whether the HLCs generated enzyme-producing cells. After injection of these stimulated HLCs, the titer of serum bilirubin in the recipient rats was markedly reduced over a long time course (6.80+/-0.93 to 4.87+/-0.22 mg/dl after 1 month and 3.52+/-1.33 mg/dl after 6 months). The results of the present study indicate that HLCs have different populations than splenic cells, and ischemia-reperfusion of the liver increased their proliferative activity. HLC transplantation successfully reduced high bilirubin levels over a long time course.

Animals↗
PubMed2004

c-Fos expression in the rat cerebral cortex during systemic GvH reaction.

OBJECTIVE: It is becoming clear that the CNS receives signals from the peripheral immune system. In order to identify the areas of the brain that receive information about a specific immune response to allogeneic antigens, we studied the expression of c-Fos, a neural activation marker, in the cerebral cortex following the induction of a graft-vs.-host reaction (GvHR) in rats. METHODS: C-Fos expression in the brain was studied by immunohistochemistry. GvHR was induced in (WKY x PVG)F(1) rats by injecting 5 x 10(8) spleen cells from PVG rats. Control rats received syngeneic cells. RESULTS: No c-Fos immunoreactivity (IR) was observed in animals undergoing GvHR in the nucleus tractus solitarii (NTS), the locus coeruleus (LC), the organum vasculosum of lamina terminalis (OVLT), the paraventricular nucleus (PVN) or the central amygdaloid nucleus (Ce). In contrast, 3 days after GvH induction c-Fos IR was observed in the piriform cortex and several other olfactory-related regions indicating the stimulation of the olfactory pathway during GvHR. Strong c-Fos IR was also observed in the occipital visual cortex of animals undergoing a GvHR, suggesting that GvHR can affect visual functions. In addition, GvHR induced c-Fos IR in the prefrontal cortex (Cg3, orbital cortex), a region that has interconnections with most sensory modalities. Double-staining studies indicate that the cells that express the c-Fos signal are neurons. CONCLUSION: We have defined the distribution of brain neurons that are affected during the induction phase of GvHR. Our results also indicate that the integration and processing of information from the immune system at CNS levels involve different areas during different types of immune responses.

Animals↗
PubMed2005

The current status of gene therapy in autologous transplantation.

Autologous hematopoietic cells have been used as targets of gene transfer, with applications in inherited disorders, cell therapy, and acquired immunodeficiency. The types of cells include hematopoietic progenitor cells, lymphocytes, and mesenchymal stem cells. The inherited disorders thus far approached in clinical trials include severe combined immunodeficiency, common variable gamma-chain immunodeficiency, chronic granulomatous disease, and Gaucher disease. Preclinical studies are vigorously under way in thalassemia, sickle cell anemia, Wiskott-Aldrich syndrome and Fanconi anemia. Clinical trials of immunological therapy with gene-modified lymphocytes are under study in the treatment of malignancies. Clinical trials using anti-viral strategies for HIV infection in combination with autologous transplantation have begun, with additional approaches being developed. Gene therapy vectors are being developed to eliminate tumor cells contaminating autologous stem cell products. However, the risk of insertional mutagenesis and the potential for development of leukemia was highlighted by the first gene therapy trials in inherited immunodeficiency syndromes that achieved a therapeutic effect. Despite the slow progress of the field to date, there is extraordinary promise for gene therapy in the future.

Animals↗
PubMed1988

Autolymphocyte therapy: previous experience and future prospects.

Autolymphocyte therapy is outpatient medical treatment for selected patients, in which a relatively small amount of white blood cells is removed temporarily from the patients, modified in the laboratory through sophisticated biotechnology, and returned to the patient for the purpose of enhancing the immune system and contributing to improved health. We suggest that autolymphocyte therapy might be a useful approach in the prevention or treatment of several diseases. Previous work with autolymphocyte therapy in the treatment of metastatic renal cell carcinoma has demonstrated that this approach is minimally toxic and biologically active. Further clinical trials are justified and currently taking place.

Antigens, Neoplasm↗
PubMed1977

The migration of lymphocytes across specialized vascular endothelium. III. Concanavalin A delays lymphocytes in normal traffic areas.

Radioactively labelled rat lymphocytes were treated in vitro with concanavalin A (con A) and injected intravenously into syngeneic recipients. By examining the blood and tissues at intervals from 30 min to 48 h after injection, it was confirmed that con A altered the distribution of lymphocytes. Comparison was made with the localization of alternatively labelled untreated lymphocytes injected into the same recipients and with untreated lymphocytes injected into other recipients. Within 1 h of injection there was a surplus of treated cells in the lungs and liver and deficits (of equal magnitude) in the blood, spleen and lymphonodes. By 24 h after injection there was a twofold surplus of treated cells in the spleen but a persisting deficit in lymphnodes. These perturbations can be ascribed to the prolonged retention of lymphocytes in normal sites of localization; there is no evidence that con A either hinders the migration of lymphocytes from the blood or diverts them to abnormal sites. It is not clear whether the delay in the recipients' tissues requires an active response to con A but, if so, then it does not proceed to blastic transformation.

Animals↗
PubMed1996

T cells, graft-versus-host disease and graft-versus-leukemia: innovative approaches for blood and marrow transplantation.

Allogeneic bone marrow transplantation is most commonly used as treatment for leukemia. Allotransplantation is associated with several interrelated immunologic processes, graft rejection, graft-versus-host disease (GvHD) and graft versus leukemia (GvL). Graft rejection can be overcome by intensive pretransplant immunosuppressive therapy. Following transplantation, immunoreconstitution must occur from donor-derived progenitors and GvHD may occur from reactivity of donor-derived immunocompetent cells against host tissues. In a related, but distinct process, donor immunocompetent cells may react against the recipient leukemia and recent data confirm that this GvL effect plays a critical role in preventing posttransplant relapse. This report summarizes present data regarding the mechanism of these processes. A major challenge is to separate the beneficial GvL effect from GvHD, the major complication of allogeneic marrow transplantation. We summarize data regarding innovative approaches to modify the composition of the transplanted marrow to optimize clinical outcome as well as use of donor lymphocyte infusions as a means to induce posttransplant GvL.

Bone Marrow Transplantation↗