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PubMed1991

Development of a treatment regimen for human cytomegalovirus (CMV) infection in bone marrow transplantation recipients by adoptive transfer of donor-derived CMV-specific T cell clones expanded in vitro.

CMV infection represents a major cause of morbidity and mortality in immunosuppressed bone marrow transplant (BMT) recipients. Life-threatening CMV infection was found to occur only in patients who did not develop a CMV-specific CD8+ Tc response. Therefore, methods to clone and expand CMV-specific Tc were developed to facilitate analysis of the specificity of the CD8+ Tc response to CMV responsible for protective immunity in seropositive donors, and to permit adoptive transfer of in vitro expanded CMV-specific Tc derived from bone marrow donors into immunocompetent HLA-matched BMT recipients to augment resistance to CMV. The immunodominant class I-restricted Tc response present in healthy seropositive individuals was found to be specific for a conserved CMV antigen introduced into the cytoplasm and presented shortly following viral penetration and uncoating, and did not require endogenous viral gene expression and protein synthesis. Thus, the protective immune response to CMV mediates lysis of virally-infected cells prior to virion assembly. Processing of viral proteins and access to presentation in the context of class I MHC molecules immediately following infection of target cells was selective for internal virion proteins, such as the tegument protein pp65. By contrast, presentation by infected cells of GB, the major CMV envelope protein, or IE, the major regulatory protein, was delayed due to a requirement for endogenous synthesis in infected cells, and CD8+ Tc specific for these proteins were detected in low frequency as compared to the immundominant response.

Antigens, Viral↗
PubMed1992

Exogenous administration of IL-1 alpha inhibits active and adoptive transfer autoimmune diabetes in NOD mice.

Diabetes susceptibility in non-obese diabetic (NOD) mice may involve immune dysregulation resulting from cytokine deficiencies. The cytokine IL-1 plays a role in various immune as well as endocrine responses and may be hypoexpressed in NOD mice. Treatment with low levels of exogenous IL-1 alpha for 22 weeks prevented the naturally occurring insulitis and diabetogenic process in NOD mice during and at least 33 weeks after cessation of IL-1 alpha treatment. Treatment with IL-1 alpha also inhibited insulitis and hyperglycemia induced by adoptive transfer of pathogenic, polyclonal CD4+8- T cells. Even after islet-cell destruction, IL-1 alpha injections in diabetic NOD mice normalized plasma glucose levels when administered in combination with insulin, whereas equivalent levels of IL-1 alpha alone did not. Our studies support the hypothesis that IL-1 alpha suppresses autoimmune diabetes and hyperglycemia in NOD mice by pleiotropic effects on both immune and metabolic systems. Thus, IL-1 treatment could clinically be an effective immunotherapeutic modality for autoimmune diabetes mellitus by suppressing early disease progression or normalize plasma glucose levels when insulin is present.

Animals↗
PubMed1982

Adoptive transfer of immunity to Plasmodium berghei with spleen cells from drug cured mice.

Plasmodium berghei infection gives rise to a fatal fulminating parasitaemia in mice. Resistance to the infection can be achieved if the mice are allowed to recover from the blood-induced infection by administration of chloroquine. In CBA/Caj, one cycle and in Balb/c mice, at least, two cycles of infection, alternating with drug-cure were necessary for the establishment of immunity. No parasitaemia was seen following further challenges after the third infection. Adoptive transfer of spleen cells from the immune mice showed that immunity could be transferred by 50 to 70 x 10(6) cells. On challenge the recipients develop high parasitaemia which was cleared in less than 5 weeks. Recipient mice given low number of spleen cells did not survive. The transfer of immune spleen cells depleted of either T or B lymphocytes abrogated the protective effect. Comparatively T lymphocytes were less effective in transferring protection than B lymphocytes. The study suggests that both humoral and cell-mediated effector mechanisms are needed for the maintenance of immunity in drug-cured immune mice.

Animals↗
PubMed1994

Protection against adoptive transfer of autoimmune diabetes mediated through very late antigen-4 integrin.

The very late antigen-4 (VLA-4) integrin expressed on the surface of lymphocytes and macrophages can regulate their migration to inflammatory sites as well as control cellular activation. The role of VLA-4 in the establishment of autoimmune diabetes is not easily predicted given the multiplicity of adhesion pathways and their differential use by various cell types. The contribution of VLA-4 to insulin-dependent diabetes mellitus was investigated by administration of VLA-4-specific monoclonal antibodies (MoAb) in an adoptive transfer model of disease in NOD mice. This study shows that VLA-4-specific MoAbs profoundly inhibit the development of diabetes with protection sustained by repeated MoAb exposure. Insulitis was completely inhibited during treatment and progressed to a severe degree once MoAb treatment was suspended, yet approximately 40% of treated recipients failed to become diabetic during 1-2 months post-treatment. Although we cannot rule out depletion of a relatively minor subpopulation of cells by prolonged anti-VLA-4 MoAb exposure, this inhibition of diabetes onset by treatment with MoAbs to VLA-4 supports a dependence on VLA-4 for cellular functions leading to diabetes and demonstrates that a significant disease modifying effect can be mediated by targeting the VLA-4 integrin.

Animals↗
PubMed1983

In vitro propagation of antigen-specific T lymphocytes that adoptively transfer resistance to Listeria monocytogenes.

Murine T cells generated against heat-killed Listeria monocytogenes or Listeria intracellular product (LIP) were propagated in a source of Interleukin 2. Both T-cell cultures were greater than 98% Lyt 1+, 2/3- and proliferated specifically against LIP and L. monocytogenes crude whole-cell antigen in vitro. Proliferation of both T-cell cultures required the presence of antigen and accessory cells syngeneic to the T cells at the left end of the major histocompatibility complex. The ability of these cultures to adoptively transfer protection against challenge with viable Listeria cells was dramatically different. As few as 10(6) LIP-specific T cells conferred significant protection against a lethal challenge of Listeria cells, whereas cultures induced against crude whole-cell antigen showed little or no protective function. The resistance conferred by LIP-specific T cells was specific in that the cells did not reduce the mortality seen after challenge with Salmonella typhimurium.

Animals↗
PubMed1980

Adoptive transfer of immunity to dysentery bacilli with immune T lymphocytes from mice orally immunized with Shigella sonnei bacilli.

It has been found previously that live virulent dysentery bacilli administered orally into mice induced immunity against subsequent infection of the animals with lethal dose of these organisms introduced i.v. The experiments revealed that this immunity could be transferred with spleen cells. This report shows that treatment with antiserum prepared against the mouse theta antigen, in the presence of complement, abrogated the ability of specific immune cells to protect the recipient mice against lethal infection with dysentery bacilli. However, treatment of the cells with anti-immunoglobulin serum, in the presence of complement, did not affect the capacity of the immune cells in the adoptive transfer experiments to protect the recipients against dysentery bacilli. Thus, T cells are required for the development of the cell mediated response occurring after oral immunization of mice with live pathogenic bacilli.

Administration, Oral↗
PubMed1991

Adoptive transfer of natural killer cell activity in B6D2F1 mice challenged with Salmonella typhimurium.

The purpose of this study was to extend our previous findings as to the role of murine NK cells in host protection to a challenge infection with virulent Salmonella typhimurium SR-11. B6D2F1 mice were depleted of NK cells with anti-asialo GM1 or a monoclonal antibody, anti-NK 1.1, followed by a salmonellae challenge. Significantly decreased numbers of splenic bacteria (P less than 0.005) in the NK cell-depleted mice were note at 12, 24, and 48 hr postchallenging, compared to the sham-injected control animals. When Percoll gradient-enriched large granular lymphocytes (NK cells) were adoptively transferred to NK cell-depleted mice followed by challenging, the splenic bacterial numbers were comparable to those present in NK cell-intact, control mice. These data indicate that large granular lymphocytes (NK cells) are responsible for the down-regulation of the protective host response in mice challenged with the facultative intracellular parasite. S. typhimurium.

Animals↗
PubMed1982

Adoptive transfer of modulation of granuloma formation and hepatosplenic disease in murine schistosomiasis japonica by serum from chronically infected animals.

The course of disease due to Schistosoma japonicum in C57BL/6J mice was examined. Animals infected with 25 cercariae of the Philippine strain of S. japonicum for 9 wk develop a peak portal hypertension of 13 +/- 0.6 cm H2O and mean hepatic granuloma area of 459 X 10(3) micrometers 2. By 30 wk, disease manifestations were reduced; mean portal pressure was 7 +/- 0.5 cm H2O and mean hepatic granuloma area was 12 X 10(3) micrometers 2. Adoptive transfer of serum but not 1 X 10(8) spleen or 4 X 10(7) lymph node cells from chronically infected mice resulted in lowering portal pressure and decreasing granuloma size in recipients. Granuloma formation in the sensitized lung model was also suppressed by serum from chronically infected mice. The immunosuppressive component of this serum was localized in the IgG1 fraction.

Acute Disease↗
PubMedDate not supplied

Induction of transient arthritis by the adoptive transfer of a collagen II specific Th1 clone to HLA-DR4 (B1*0401) transgenic mice.

Collagen II arthritis (CIA) represents an animal model of human RA that can be induced in DBA/1J (H-2(q)) but not in C57BL/6 mice (H-2(b)). A vigorous CII specific CD4 Th1-cell response but not IgG2 anti-CII antibody or CIA could be induced in C57BL/6 mice made transgenic for the RA shared epitope DR4 (B1*0401). We developed CD4 Th1-cell clones specific for CII from these transgenic (tg) mice in order to determine if the adoptive transfer of these clones into syngeneic tg C57BL/6 recipients could induce CIA. Three bovine CII specific (bCII) CD4 Th1-cell clones and one T-cell line specific for an immunodominant region of bCII (p261-273) were generated. Among these only one clone that could up-regulate anti-CII, IgG2 antibody in the recipient mice was able to induce transient arthritis. However, this level of IgG2 anti-CII antibody was only one-third of that seen in CII immunized DBA/1J mice that develop persistent arthritis. These results confirm our previous observations that the induction of CIA requires a sustained IgG2 antibody response to CII, an effect difficult to achieve even in DR4 (B1*0401) tg mice reconstituted with CD4 Th1 cells. This suggests that a rate limiting step in the development of human RA among those individuals expressing the RA shared epitope may be the requirement to generate sustained levels of complement fixing antibody to arthritogenic antigens.

Animals↗
PubMed1985

Adoptive transfer of murine host protection to salmonellosis with T-cell growth factor-dependent, Salmonella-specific T-cell lines.

A spent medium antigen was prepared from the avirulent RIA strain of Salmonella typhimurium. Lymph node cells isolated from female BALB/c mice injected subcutaneously with the spent medium antigen exhibited antigen-specific proliferation. By using these cells and T-cell growth factor, continuous spent medium antigen-specific, Thy 1.2-sensitive lines were generated. These cells exhibited antigen-specific proliferation in vitro and were effective in inducing significant (P less than 0.01) host protection when adoptively transferred to naive syngeneic mice.

Animals↗
PubMed1991

Establishment of cell-to-cell contact by adoptively transferred adherent lymphokine-activated killer cells with metastatic murine melanoma cells.

A murine model of pulmonary B16 melanoma was used to study the infiltration into metastases of lymphokine-activated killer (LAK) cells and adherent lymphokine-activated killer (A-LAK) cells and, specifically, to study whether A-LAK cells are able to leave the tumor microcirculation and establish cell-to-cell contact with malignant cells. Fluorescence microscopy demonstrated that A-LAK cells accumulated in metastases twice as efficiently as LAK cells during interleukin-2 stimulation. Electron microscopy of pulmonary metastases 16 hours after administration of 2.5 x 10(7) A-LAK cells revealed A-LAK cells, identified by the presence of typical two-compartment granules, in direct contact with melanoma cells. This finding was confirmed by using A-LAK cells prelabeled with polycationized ferritin. In conclusion, our observations demonstrate unambiguously the ability of adoptively transferred A-LAK cells to establish contact with extravascular metastatic melanoma cells.

Animals↗
PubMed1981

Adoptive transfer of immunity to infection with Theileria parva (East Coast fever) between cattle twins.

Resistance to a lethal challenge with Theileria parva (Muguga) was transferred between two pairs of chimeric bovine co-twins with 5 to 9 X 10(10) syngeneic thoracic duct leucocytes from the immunised partner. In one recipient, the infection became established and was eliminated. In the second recipient, the disease did not become patent. Both recipients were immune to a second challenge of T parva (Muguga). The results confirm both that chimeric twin calves are suitable as a model for the adoptive transfer of cell-mediated immunity in cattle and that recirculating lymphocytes confer resistance against infection with T parva to immune cattle.

Animals↗
PubMed1991

Adoptively transferred tumor-infiltrating lymphocytes can cure established metastatic tumor in mice and persist long-term in vivo as functional memory T lymphocytes.

Tumor infiltrating lymphocytes (TILs) are derived from solid tumors by culturing single cell suspensions of the tumors in low dose interleukin-2 (IL-2) and intermittent tumor stimulation. We have investigated the survival of TILs after intravenous injection into tumor-bearing mice. Using several murine transplantable sarcomas, we examined the in vivo survival of TILs derived from B6.PL Thy 1a/CY mice (Thy-1.1), which were used to treat established experimental metastases in C57BL/6N (Thy-1.2) mice. Donor and host lymphoid cells could be clearly distinguished by fluorescence-activated cell sorting. We found that TILs or TILs + IL-2 could extend the survival of and, in some instances, cure established experimental hepatic and pulmonary metastases. Donor TILs could be recovered from treated animals at all time points tested; in mice cured of pulmonary metastases donor TILs could be detected as late as 119 days after intravenous injection even in the absence of exogenous IL-2. The administration of a relatively low dose of IL-2 in vivo to mice receiving TILs increased the number of donor TILs recovered from the lungs of cured animals 5-10-fold at all time points but did not change the period of time during which donor TILs could be detected in vivo. Additionally, TILs could be recovered from animals cured of established metastases and such cells retained their antitumor activity in vivo. Finally, when mice cured of pulmonary metastases by TILs or TILs + IL-2 were rechallenged with tumor, donor TILs specifically accumulated at the site of tumor rechallenge up to 4 months after adoptive transfer of TILs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Adoptive transfer of mast cells does not enhance the impaired survival of Kit(W)/Kit(W-v) mice in a model of low dose intraperitoneal infection with bioluminescent Salmonella typhimurium.

Mast cells are important effector cells in IgE-associated immune responses, but also can contribute to host defense in certain examples of bacterial infection. We found that genetically mast cell-deficient WBB6F1-Kit(W)/Kit(W-v) mice exhibited more bacterial CFUs per spleen by 6 days after intraperitoneal injection of bioluminescent Salmonella typhimurium, and died more rapidly after infection, than did the congenic WBB6F1-Kit(+/+) wild type mice. Adoptive transfer of bone marrow-derived cultured mast cells of Kit(+/+) origin to the peritoneal cavity of Kit(W)/Kit(W-v) mice resulted in engraftment of mast cells in the peritoneal cavity and mesentery of the recipient mice, and the development of large numbers of mast cells in the spleen. However, such mast cell-engrafted Kit(W)/Kit(W-v) mice appeared sicker after intraperitoneal injection with S. typhimurium than did mast cell-deficient Kit(W)/Kit(W-v) mice, and exhibited numbers of CFUs of bacteria per spleen, and a survival curve, that were not significantly different than those of Kit(W)/Kit(W-v) mice. These results, when taken together with prior studies investigating the roles of mast cells in innate immunity, strongly suggest that whether mast cells can be shown to have a significant role in enhancing survival during bacterial infections may depend critically on the details of the particular experimental systems examined.

Animals↗
PubMed2004

Characterization of colonic and mesenteric lymph node dendritic cell subpopulations in a murine adoptive transfer model of inflammatory bowel disease.

Ulcerative colitis and Crohn's disease, collectively termed inflammatory bowel diseases (IBD), are chronic inflammatory diseases of the intestine that afflict more than 4 million people worldwide. Intestinal inflammation is characterized by an abnormal mucosal immune response to normally harmless antigens in the gut flora. In Crohn's disease, the pathogenic mucosal immune response is a typical T helper (TH1) type cell response, whereas ulcerative colitis is predominantly associated with a TH2 response. We are interested in the role of dendritic cells in early immunologic events leading to T cell activation and chronic intestinal inflammation. Using a murine adoptive transfer model of IBD, we found an accumulation of dendritic cells in colon and mesenteric lymph nodes during the early stage of IBD before the appearance of epithelial lesions and tissue degradation. In situ immunostaining and flow-cytometric analysis revealed that approximately 50% of colonic dendritic cells were CD11b B220 myeloid dendritic cells and 50% expressed the CD11b B220 plasmacytoid phenotype. In corresponding mesenteric lymph nodes, approximately 16% were plasmacytoid dendritic cells. Colonic myeloid dendritic cells were shown to express the co-stimulatory molecule CD40. Both, colonic myeloid and plasmacytoid dendritic cells released interferon-alpha in situ and stimulated T cell proliferation ex vivo. Our results show that dendritic cells can mature in the intestine without migrating to mesenteric lymph nodes. Mature intestinal dendritic cells may form a nucleation site for a local T cell response and play an important role in the pathogenesis of IBD.

Animals↗
PubMed1983

Adoptive transfer of resistance to growth of an idiotype-secreting hybridoma by T cells from idiotypically suppressed mice.

A/J or CAF1 mice that are suppressed with respect to an idiotype, CRIA, associated with anti-Ar antibodies, and hyperimmunized develop high concentrations of idiotype-suppressor T cells. In this paper we show that such CAF1 mice are resistant to the growth of a CRIA-positive hybridoma that is lethal in normal or in immunized non-suppressed mice. No resistance was observed to the growth of a hybridoma secreting anti-Ar antibodies that lack CRIA. The state of resistance could be adoptively transferred to naive syngeneic recipients with spleen cells or T-enriched spleen cells from suppressed hyper-immunized mice; B-enriched cells were ineffective.

Animals↗
PubMed1996

Establishment of anti-Epstein-Barr virus (EBV) cellular immunity by adoptive transfer of virus-specific cytotoxic T lymphocytes from an HLA-matched sibling to a patient with severe chronic active EBV infection.

We describe an experience of a specific immune transfer treatment in a patient with chronic active EBV infection. The patient had low anti-EBV T cell-mediated cytotoxic activity in his peripheral blood mononuclear cells (PBMC), which may have been the primary cause of the disease. An EBV-specific cytotoxic T lymphocyte (CTL) line was established from PBMC obtained from the patient's sister whose human leucocyte antigens (HLA) are identical to patient's. The patient received three courses of intravenously administered CTL at 3-week intervals. The number of the cells was increased with each course of treatment. After infusion of the T cell line, anti-EBV CTL activity was detected in the patient's PBMC. CTL activity increased markedly after the second course of immune transfer therapy. The amount of EBV DNA in the patient's plasma showed transient but repeated decreases. Serum levels of tumour necrosis factor-alpha (TNF-alpha), which had elevated before treatment, began to decrease after initiation of treatment. No adverse effects were directly associated with CTL infusions. Despite having previously received a pneumococcal vaccine and prophylactic antibiotics, the patient died of infection caused by Streptococcus pneumoniae bacteraemia 27 days after the third infusion. Although the long-term efficacy and safety of this therapy remains to be established, our findings suggest that adoptive transfer of CTL specific for EBV obtained from an HLA-matched donor might be a promising treatment for patients with chronic active EBV infection.

Child↗
PubMed1984

Evaluation of Mycobacterium leprae immunogenicity via adoptive transfer studies.

The immune response of mice to live, heat-killed, or autoclaved Mycobacterium leprae was investigated. After sensitization with 10(7) organisms in each group, recipient mice were transfused with the sensitized splenocytes 28 days later. A selected number of these mice were infected with 5 X 10(3) M. leprae, and the remaining animals were sacrificed at scheduled intervals for evidence of cell-mediated immunity to the M. leprae cell extract. Data from these and the bacteriological assays showed that all three materials induce cell-mediated immunity and also extend protection against the M. leprae challenge but not against a Listeria monocytogenes challenge. Adoptive immunity against M. leprae was expressed equally effectively in both non-irradiated animals and those sublethally (500 R) irradiated. This study reveals that, after adoptive transfer of immunity, a bacillary restriction occurs with concomitant onset of delayed hypersensitivity and that the protection observed could be specifically directed against an M. leprae challenge.

Animals↗