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PubMed1987

Functional activity in vivo of effector T cell populations. III. Protection against Moloney murine sarcoma virus (M-MSV)-induced tumors in T cell deficient mice by the adoptive transfer of a M-MSV-specific cytolytic T lymphocyte clone.

The functional activity of Moloney murine sarcoma virus (M-MSV)-specific T lymphocytes in vivo was assayed by the i.v. injection of virus-specific T lymphocytes into T cell-deficient "B mice". Virus-specific T lymphocytes generated in mixed lymphocyte tumor cell cultures were transferred i.v. into syngeneic "B mice" injected simultaneously at a distant site with the virus. These experiments indicated that a low dose (1 X 10(6) cultured cells) of infused lymphocytes can afford protection. To define the T lymphocyte subpopulation which was active, Lyt-2+ lymphocytes were selected by "panning" on plastic petri dishes coated with anti-Lyt-2 monoclonal antibody, and Lyt-2- lymphocytes selected by treatment with anti-Lyt-2 monoclonal antibody and complement. The results indicated that a Lyt-2+ lymphocyte-enriched population was more efficient in conferring protection against M-MSV-induced tumors. To investigate if cytolytic T lymphocytes (CTL) alone had a protective effect, a M-MSV-specific CTL clone was transferred in the same model system. The results demonstrated that a M-MSV-specific CTL clone prevented M-MSV-induced tumor growth and also induced the destruction of syngeneic Moloney murine leukemia virus (M-MuLV)-induced MBL-2 leukemic cells in the peritoneal cavity. However, the cell dose required to obtain protection using a CTL clone was higher than that which was effective when mixed lymphocyte tumor cell culture cells were used. To assess the ability of the transferred cells to home and to repopulate the lymphoid organs of the "B mice", the frequency of virus-specific CTL precursors in the spleen was evaluated by limiting dilution analysis. The results indicated that lymphocytes from mixed lymphocyte tumor cell cultures can be recovered from the spleens of "B mice" injected i.v. 25 days earlier. On the contrary, following the transfer of an active CTL clone, a very low frequency (less than 1/200,000 cells) of virus-specific CTL precursors was present in the spleens of recipient animals. The same M-MSV-specific CTL clone did not yield protection against M-MSV-induced tumors or MBL-2 leukemic cells when injected i.v. into M-MuLV tolerant mice.

Animals↗
PubMed1993

Evidence for a preferential V beta usage by the T cells which adoptively transfer diabetes in NOD mice.

Non-obese diabetic (NOD) mice become spontaneously diabetic as a result of a genetically programmed autoimmune process mediated by autoreactive T lymphocytes and directed against beta cell antigen(s). Studies dealing with T cell receptor (TcR) variable (V) gene usage by such autoreactive T lymphocytes have given contrasted results. Various reasons may explain these discrepancies: the multiplicity of antigenic epitopes putatively recognized by T cells, the ambiguity between specifically committed T cells and passenger lymphocytes homing randomly to the pancreas, the necessarily limited size of the T cell clone panels which have been analyzed for TcR rearrangements and, last but not least, the flexibility of T cell repertoires. To circumvent some of these difficulties, we have decided to concentrate upon the T cell population present in diseased animals and capable of transferring diabetes into young naive NOD recipients. This population, composed of CD4+ and CD8+ T cells, is presumably committed against the relevant beta cell antigens and is the most likely to reveal a bias in V gene usage if such a bias does indeed exist. To find out whether certain V beta genes are more frequently used than others by such pathogenic T cells, T lymphocytes from diabetic donors have been depleted in vitro of defined V beta subsets before being reinoculated into permissive recipients. Out of four V beta families probed under such conditions, three (V beta 8, V beta 5 and V beta 11) are neutral. Their absence neither increases nor reduces the final incidence of successful transfers, indicating that these gene segments are not preferentially used. In contrast, the depletion of V beta 6-positive T cells results in a severe reduction of transfers, suggesting that V beta 6 gene is used with a relatively high frequency by diabetogenic CD4+ and/or CD8+ T cells. To define more precisely which subset uses V beta 6 gene preferentially, we have performed mixing experiments with deleted and intact subsets. The results, based on disease transfer and insulitis severity, indicate that the V beta 6 bias affects predominantly the CD4+ subset. Thus, at variance with several studies concluding that V gene usage in NOD mice is heterogeneous, our present data suggest that disease transferring T cells use a relatively restricted set of V beta genes.

Animals↗
PubMed1995

Resident microglia and hematogenous macrophages as phagocytes in adoptively transferred experimental autoimmune encephalomyelitis: an investigation using rat radiation bone marrow chimeras.

Hematogenous macrophages are known to be involved in the induction of tissue damage in the central nervous system (CNS) as well as of clinical symptoms in experimental autoimmune encephalomyelitis (EAE). Although resident microglia can become phagocytic under certain circumstances, little is known about the role of these cells in brain inflammation in vivo. We thus studied EAE in the model of radiation bone marrow chimeras that allows us to distinguish donor-derived hematogenous cells from resident effector cells. Inflammation in the CNS was qualitatively and quantitatively similar in chimeras compared to fully histocompatible Lewis rats. Although activated resident microglial cells were outnumbered four- to sevenfold in EAE lesions by hematogenous macrophages, the number of resident microglia with ingested myelin was equal to that of macrophages containing myelin debris. Phagocytic resident microglia, expressing the macrophage activation marker ED1, showed ramified as well as amoeboid morphology. From our studies the following conclusions can be drawn. First, a considerable proportion of resident microglia upregulated ED1. Second, resident microglia provide a small but substantial source of brain macrophages in EAE as compared to the large influx of macrophages. Third, our results suggest that microglia, due to their strategic position within the CNS, are more effective in removal of myelin debris compared to hematogenous macrophages.

Animals↗
PubMed1980

The effect of bursectomy on the adoptive transfer of resistance to Marek's disease.

Immunization with inactivated viral antigens protected chickens against Marek's disease. Non-immunized chickens could be protected by injections of spleen cells but not of serum from immunized, histocompatible donors. Chickens rendered agamma-globulinaemic by bursectomy and irradiation could also be immunized against Marek's disease by inoculation with viral antigens, but spleen cells from these immunized, bursectomized and irradiated donors did not confer protection on the recipients into which they were injected. It was concluded that, although in the bursectomized, immunized donors cell-mediated immunity alone was able to provide a fair degree of protection against Marek's disease, the protection afforded against the disease by spleen-cell transfer was at least partly attributable to the transfer of antibody-producing cells, and that humoral immunity, while not being an absolute requirement for resistance, is normally an important component of the resistance mechanism.

Animals↗
PubMed1981

Adoptive transfer of immunity induced by semi-allogeneic hybrid cells, against a murine fibrosarcoma.

Semi-allogeneic somatic hybrid cells derived from the fusion of a C57BL/6 fibrosarcoma (MCB6-1) and A9 cells (C3H origin) were used to immunize C57BL/6 mice against the parental tumor cells. These hybrid cells expressed H-2 histocompatibility antigen of both parental cells (H-2b and H-2k), and failed to produce tumors in normal C57BL/6 mice. A single i.p. injection of hybrid cells induced anti-tumor immunity which could be transferred to normal C57BL/6 recipient mice by immune spleen or peritoneal cells; the efficient cells were T cells, as this activity was completely abrogated by treatment with anti-Thy-1-2 antiserum and complement. Among immune splenic T cells, only the light-density T cells, obtained after fractionation on Percoll gradient, were effective in the transfer of immunity. Immunity induced by the hybrid cells was specific for MCB6-1 parental tumor cells. This immunity could be transferred during two brief periods, 7 to 12 days, and 40 to 50 days, after hybrid cell injection; there appeared to be an intermediate period, 12 to 40 days after immunization, during which no immunity could be transferred. These results suggest a suppressive mechanism implicated during hybrid cell immunization and interacting with the anti-tumor immune response.

Animals↗
PubMed1981

In vivo anti-tumor effects of local adoptive transfer of mouse and human cultured lymphoid cells.

Mouse and human lymphoid cells were cultivated in the presence of T-cell growth factor (TCGF) and evaluated for their in vivo anti-tumor effect in mice. Cultured spleen cells of normal BALB/c mice or of mice bearing the M109 tumor had a high level of cytotoxic activity in vitro against a variety of tumor target cells and had characteristics of natural killer cells. These cultured cells were evaluated for their in vivo cytotoxic activity by a mixture with [125I]dUrd-labelled M109 tumor cells (2 x 10(5)) at a 30:1 ratio and inoculation of the mixture into the footpads of BALB/c mice. The level of radioactivity remaining in the footpad was determined at various periods following inoculation of radiolabelled tumor cells. The presence of cultured cells in the inocula caused a marked decrease in the footpad radioactivity by 24 h. However, the slope of clearance of the radiolabel then became similar to that in the control mice. The cultured cells delayed, but did not prevent, tumor appearance, and did not influence the subsequent rate of growth of the tumors. The transient effects of the cultured cells contrasted with the more prolonged in vivo effects of alloimmune lymphocytes, and this may be due to their short survival period. Ninety-nine percent of [125I]dUrd-labelled cultured mouse lymphoid cells were eliminated within 48 h of i.f.p. inoculation. Cultured human lymphoid cells, initiated from the blood of normal donors, also had a high level of cytotoxic activity in vitro and were evaluated for their in vivo effects by intra-footpad inoculation into nude mice, together with radiolabelled human tumor cell lines, G-11 or HT-29. In vivo cytotoxic activity of the human cultured lymphoid cells correlated with their cytotoxic effect in vitro. These results indicate that cultured mouse an human effector cells have appreciable in vivo cytotoxic effects against tumor cell lines. However, the transient duration of these effects may limit their immunotherapeutic potential.

Animals↗
PubMed1985

Systemic adoptive transfer of immunity and low-dose irradiation eradicate metastases of 13762A rat mammary adenocarcinoma.

Rats cured of poorly immunogenic 13762A tumor by a combination of surgery and cyclophosphamide (CY) treatments produced peritoneal exudate cells (PEC) that prevented tumor growth when transferred to naive recipients, but they were ineffective against established tumor. A highly immunogenic 13762A clone (18A) induced PEC lymphocytes that completely reversed the growth of established primary tumor and of lymph-node metastases. 18A-immune PEC alone strongly inhibited tumors of 7 days' duration, but only moderately suppressed 14-day tumors, and had no effect on 21-day tumors. Irradiation (450 R) of rats prior to tumor transplantation improved the effectiveness of the PEC given at 7 days, but the benefit had gone by 14 days. Long-term T-cell depletion prior to tumor challenge allowed PEC inhibition of 7- and 14-day tumors, but not 21-day tumors. The most potent strategy was the administration of 450 R followed immediately by immune PEC. When rats with 21-day tumors were so treated, the metastases grew temporarily to a maximum diameter of 2-5 cm and then completely regressed. We concluded that a combination of immune T cells and 450 R can cure established, massive metastases, probably through a combination of an increase in the numbers of T-cell effectors and elimination of suppressor cells.

Adenocarcinoma↗
PubMed1987

Inhibition of murine lymphoma growth by adoptive transfer of lymphocytes sensitized to a xenogenized tumor variant.

Lymphocytes immune to a highly immunogenic ("xenogenized") variant of a murine lymphoma--which were shown to exert anti-xenogenized tumor activity in a previously described model of tumor immunotherapy--were tested in the present study for possible suppressive effects on the growth of an i.c. graft of the original lymphoma. Remarkable tumor-inhibitory effects followed the i.v. infusion of splenic lymphocytes sensitized or restimulated in vitro, or derived from animals immunized in vivo with the xenogenized tumor cells. The pattern of inhibition of the parental cells was apparently similar to that previously described for the xenogenized variant, but preliminary evidence suggests that the underlying mechanisms may be different.

Animals↗
PubMed1976

Adoptive transfer of tumor immunity between twins by in vitro immunized nodal macrophages and lymphocytes: reversal of serum enhancement.

The lymphocytes and serum of a nonidentical twin male with advanced colon cancer were evaluated in vitro for their ability to inhibit the growth of autologous tumor cells. The patient's serum enhanced autologous tumor cell growth. Three siblings including an HL-A matched grade A female twin underwent similar studies. Benign lymph nodes of the twins and one sibling were evaluated for the ability of nodal macrophages to be sensitized to the patient's tumor antigen. The male twin patient received intralymphatically in vitro sensitized nodal macrophages and lymphocytes from the female twin donor. Thirty days after treatment the patient's lymphocytes and serum inhibited the growth of autologous tumor cells.

Adult↗
PubMed1995

Protective resistance to experimental Borrelia burgdorferi infection of mice by adoptive transfer of a CD4+ T cell clone.

The anti-spirochete T cell immune response to immunization with Borrelia burgdorferi was investigated. The cellular immune response to vaccination of immunocompetent BALB/c mice was characterized initially in vitro by assay of the proliferative response of primary lymph node cells to B. burgdorferi sonicate. Subsequently, an anti-spirochete T cell line (RBN2.1) and clone (97.1) were derived from lymph node cells of BALB/c mice primed with B. burgdorferi antigen. Both the line and clone were CD4+ by flow cytometric analysis. Significantly, RBN2.1 and clone 97.1 were able to transfer resistance to infection to syngeneic naive recipients. Assay of antigen-specific interleukin-2, interleukin-4, tumor necrosis factor-alpha, and interferon-gamma production demonstrated that clone 97.1 was of the Th2 subclass. When B. burgdorferi sonicate was fractionated on SDS-PAGE and then electroeluted, clone 97.1 was reactive exclusively to a spirochete protein of approximately 21 kDa. These data suggest that T-cell-mediated protective immunity to infection by B. burgdorferi can be elicited by active immunization.

Animals↗
PubMed1994

Oral administration of human insulin to NOD mice generates CD4+ T cells that suppress adoptive transfer of diabetes.

Oral administration of porcine insulin has been shown to be effective in preventing the spontaneous occurrence of diabetes in the Non-Obese Diabetic (NOD) mouse model. In the present study, we demonstrate that feeding 6-week-old female mice with 20 units of human insulin every 2-3 days for 30 days induces an active mechanism of suppression through the generation of regulatory T cells. Adult irradiated NOD males i.v. injected with 5 x 10(6) T cells from the spleens of diabetic female donors and the same number of T cells from the spleens of insulin-fed animals had less successful diabetes transfer than controls (4/15 vs. 8/16, P < 0.001). Protection from clinical diabetes was associated with a reduction in severe insulitis (16.4 +/- 3.6% vs. 52.3 +/- 12.8%, P = 0.023). However, more than 85% of the islets were inflamed. Feeding animals for 15 days reduced the magnitude of this protection since the number of successful transfers after 1 month was comparable (12/17 vs. 14/17) despite a significant delay in diabetes onset (P < 0.001). No difference in the contribution of T cell subsets was noted by cytofluorometry in the spleens of treated animals. When T cell subsets from insulin-fed animals were co-injected with diabetogenic T cells, only purified CD4+ T cells were able to transfer protection since only 3/12 mice became diabetic after 36 days in comparison to 3/6 in the group co-injected with CD4+ T cells from PBS-fed animals, or 5/6 in the group injected with CD8+ T cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Adoptive transfer of human peripheral blood lymphocytes (PBL) in scid mice.

Two protocols were examined for the ability to transfer a human T cell system into SCID mice. Upon intraperitoneal injection (i.p.) of human peripheral blood lymphocytes (PBL) into SCID mice the injected cells could be recovered over weeks from the peritoneal cavity, yet human T cells did not seed into secondary lymphoid organs such as the spleen, lymph nodes or bone marrow. In contrast, SCID mice grafted with human embryonal thymus tissue contained high numbers of CD4+CD8- and CD8+CD4- human T cells in their lymph nodes and spleen when they had been injected i.p. with human PBL.

Animals↗
PubMed1989

Evaluation of natural killer and lymphokine-activated killer (LAK) cell activity in vivo in patients treated with high-dose interleukin-2 and adoptive transfer of autologous LAK cells.

This study investigated the development of peripheral blood natural killer (NK) and lymphokine-activated killer (LAK) cell activity in vivo in cancer patients treated with high doses of recombinant interleukin-2 and autologous LAK cell infusion. It was found that interleukin-2 administration by bolus injection resulted in an early but transient rise of NK and LAK cell activity in vivo during the first 5-9 days of treatment (postpriming period), whereas continuous infusion of interleukin-2 caused an increase in both cytotoxic activities in the second phase of the treatment, concomitant with infusions of autologous LAK cells. Elevated NK but not LAK cell activity in vivo in the continuous-infusion patients persisted up to 180 days after completion of therapy. In both bolus and continuous interleukin-2 protocols, augmented NK cell activity in vivo appeared to be correlated with a beneficial response to therapy.

Adult↗
PubMed1981

Adoptive transfer of immunity to Plasmodium berghei after busulfan and cyclophosphamide treatment of recipient mice.

Balb/c mice injected with P. berghei die about 21 days after infection. Successful cell transfer in mice was made possible by the pretreatment of the recipient with a combination of busulfan and cyclophosphamide. Cell counts showed that drug-treated mice contain 20 times less bone marrow cells than normal mice, and when injected with P. berghei die significantly later than normal controls. The animals were injected with normal (NBM) and immune bone marrow and normal (NSp) and immune spleen (ISp). The results obtained showed that ISp lengthens significantly the average survival time, producing cure of 50% of the recipients. Transfer of NSp and NBM also lengthens the average survival time.

Animals↗
PubMed1981

Adoptive transfer of delayed-type hypersensitivity to Sendai virus. III. Effect of H-2 mutations on recognition by K, D-region restricted T effector lymphocytes.

The H-2 restriction pattern of cytolytic T lymphocytes (Tc) and T lymphocytes which mediate a delayed-type hypersensitivity response (Td) directed against infectious Sendai virus was investigated using H-2 mutant mice. Td and Tc lymphocytes exhibit the same fine specificity for self-recognition, for example, B6.C-H-2bm1 effector T cells were unable to recognize viral antigens in association with wild-type Kb and vice versa, B6.H-2bm6 effector cells did not mediate a reaction against virus plus wild-type Kb but, on the other hand, T cells of wild-type Kb recognized virus plus Kbm6 BALB/c-H-2dm2 T cells lacked reactivity against virus in association with wild-type Dd, but again wild-type Dd effector cells recognized virus plus Ddm2.

Animals↗
PubMedDate not supplied

Adoptive transfer of resistance to Pseudomonas aeruginosa infection by splenocytes and bone marrow cells from BALB/c mice immunized by Pseudomonas aeruginosa lectin preparations.

BALB/c mice immunized by intraperitoneal injection of purified Pseudomonas aeruginosa lectin preparations are fully protected against a lethal dose of the live bacteria. Intraperitoneal inoculation of splenocytes or bone marrow cells obtained from actively immunized mice into naive syngeneic mice was shown to significantly increase their resistance to P. aeruginosa infection. A similar transfer of splenocytes or bone marrow cells from untreated control mice did not provide protection against a lethal Pseudomonas challenge. Administration of immunocompetent cells from immunized animals to naive mice by the i.v. route was less efficient than the i.p. inoculation, probably due to different homing of the cells. Only the i.p. injection concentrated the immune cells to the site of infection.

Animals↗