PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Lymphocyte Transfusion”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 199 records · Page 11Linked to original sources
PubMed1985

Adoptive immunotherapy of a BALB/c lymphoma by syngeneic anti-DBA/2 immune lymphoid cells: characterization of the effector population and evidence for the role of the host's non-T cells.

It has been previously shown that the BALB/c lymphoma YC8 is susceptible to lysis by syngeneic anti-DBA/2 lymphocytes and that YC8-bearing BALB/c mice can be cured by adoptive transfer of such immune effectors. In this study in vivo and in vitro functions of the curative immune lymphocytes have been evaluated together with the role of the host immune system in the mechanism of tumor eradication. It was found that the curative anti-DBA/2 lymphocytes were not directly cytotoxic to YC8 cells although they developed into YC8-lytic cells after in vitro restimulation with YC8. In vivo, the immune lymphocytes were able to mediate a tumor-specific delayed type hypersensitivity reaction against YC8 but had a low tumor-neutralizing activity in the Winn assay. Proliferation of infused BALB/c anti-DBA/2 lymphocytes was necessary for the in vivo therapeutic effect, since irradiation of effector cells or treatment of the donor immune lymphocytes with vinblastine abolished their curative capacity. Immunodepression of the T cell compartment of the prospective tumor-bearing animals by thymectomy plus irradiation or its abrogation in B mice (thymectomized, lethally irradiated, and reconstituted with fetal liver cells) did not interfere with the therapeutic effect of the transferred anti-DBA/2 lymphocytes. Blocking the macrophage functions of the host by carrageenan, however, abolished the therapeutic effect of immune lymphocytes. These data indicate that a radiation-resistant, non-T cell is involved in the tumor eradication induced by anti-DBA/2 lymphocytes. It was also shown that cured mice, tested 90 days after therapy, become resistant to 5 X 10(3) LD80 YC8 cells and that this resistance was due to the presence of memory cells derived from the transferred and not from the host lymphocyte population.

Animals↗
PubMed1988

Macrophage infiltration in tumors and tumor-surrounding tissue: influence of serotonin and sensitized lymphocytes.

In a delayed-type hypersensitivity reaction serotonin released from mast cells plays an important role in the induction of a cellular infiltrate at the site of antigen challenge. In analogy, we have studied whether it is possible to enhance the number of intratumoral macrophages by injecting serotonin into a s.c. SL2 lymphosarcoma. The vessels in the tissue surrounding the tumor responded well to serotonin, as there was an influx of i.v. injected 51Cr-labeled sensitized spleen cells in this tissue during the first 4 h after intratumoral injection of serotonin. At 24 h after serotonin injection there was an influx of macrophages into this tumor-surrounding tissue. No influx of cells was detected in the tumor itself during the first hours after injection of serotonin. In the tumor, similar phenomena occurred as in the surrounding tissue, but with a delay of about 24 h. This suggests that lymphocytes leave the blood circulation in the tumor-surrounding tissue and migrate to the tumor. The influx of macrophages into the tumor after intratumoral injection of serotonin is probably due to an immunological reaction as the lymphocyte influx preceeds the macrophage influx into tumors. In addition, transfer of sensitized lymphocytes, as well as lymphocytes from a tumor-bearing host caused an enhanced influx of macrophages into the tumor. To test the specificity and serotonin dependency of the phenomenon of infiltrating cells in tumors we have used a footpad swelling assay in which the serotonin dependency and the antigen specificity of the response against syngeneic tumor cells was shown. The following picture emerged: an intratumoral serotonin injection enables lymphocytes to leave blood vessels in the tumor-surrounding tissue. These lymphocytes with specificity for tumor antigens migrate to the tumor. After contact with the antigenic tumor cells, these lymphocytes secrete chemoattractive factors for monocytes/macrophages. Also these monocytes/macrophages leave the circulation in the tumor-surrounding tissue. Subsequently the macrophages invade the tumor. We conclude that the number of intratumoral macrophages can be enhanced by serotonin.

Animals↗
PubMed1987

Specific inhibition of natural killer (NK) activity against different alloantigens.

Allogeneic lymphocyte cytotoxicity (ALC), i.e., rapid rejection of i.v. injected allogeneic lymphocytes in unprimed hosts, is an example of NK activity. Apparently anomalous rejection patterns, such as acceptance of F1 hybrid cells by parental hosts and rejection of parental cells by F1 hybrid hosts in many strain combinations, would fit the hypothesis that the effector cells in ALC recognize the absence of certain self-molecules (passwords) rather than the presence of nonself determinants. However, cold target inhibition studies showed that ALC displays allospecificity: when a mixture of radiolabeled AO and DA cells were injected i.v. into euthymic or athymic PVG rats, adding a surplus of cold DA cells reduced killing only of labeled DA cells and vice versa. Furthermore, semiallogeneic cold target cells were ineffective in inhibiting elimination of fully allogeneic cells, which supports the argument against a modification of the hypothesis that self-determinants inhibit a postbinding stage of lysis. Finally, (DA x AO)F1 cells injected into (DA x PVG)F1 hosts were rapidly rejected, despite the fact that donor and host shared expressed DA determinants. In sum, our results show that a hypothesis based on inhibition of killing by self-determinants can only be sustained with extensive modifications, and favor the alternative mechanism that the effector cells positively recognize the presence of allospecific determinants on the target cell surface.

Animals↗
PubMed1986

Polymorphic and autoreactive H-2-specific monoclonal antibody isolated after injections of syngeneic Sendai virus-coated lymphocytes.

An H-2-specific monoclonal antibody (mAb Q-1) was obtained from B10.Q (H-2q) mice injected with syngeneic Sendai virus-coated cells. The IgM monoclonal antibody recognizes the public determinant H-2.25 shared by H-2k (Kk) and H-2r haplotypes and cross-reacts with H-2d, H-2s, H-2p, and H-2q cells, the latter being the haplotype of the challenged B-cell donor. The binding of mAb Q-1 to H-2d, H-2s, H-2q, and H-2p cells was lower than to H-2k and H-2r and of decreasing affinity but could be clearly distinguished from the negative reactions with H-2b and H-2f cells. MAb Q-1 distinguishes between Sendai virus-coated and uncoated lymphocytes only cells with low-affinity binding. On virus-coated or infected (H-2p, H-2q, H-2d, H-2s) cells lysis was stronger than on normal lymphocytes. We interpret the enhanced lysis of Sendai virus-positive cells by mAb Q-1 to be due to recognition of a modified exposure of public H-2 determinants induced by Sendai virus.

Animals↗
PubMed1993

Lymphocyte engraftment conveys immunity and alters parasite development in scid mice infected with Echinococcus multilocularis.

Severe combined immune-deficient (scid) mice, which lack functional B- and T-lymphocytes, were infected with Echinococcus multilocularis larval tissue before or after reconstitution with lymphoid cells from immunocompetent donor mice. Untreated scid mice were highly susceptible to E. multilocularis infection, while scid mice reconstituted with purified lymphocytes derived from either infected or uninfected normal donor mice were capable of almost totally suppressing the growth of the larval cyst mass. The somatic development of the larval parasite varied according to the infection status of the cell donor, with protoscolices forming in scid mice reconstituted with cells from uninfected normal mice but not in those receiving cells from infected normal mice. These results confirm earlier findings that lymphocytes are important in suppressing the growth of E. multilocularis cysts in the intermediate host and also indicate that protoscolex development is influenced by lymphocytes or their products.

Animals↗
PubMed1980

Genetic resistance of CBA and A mice to transplanted lymphoid and hemopoietic cells of CBA.M523 mutants and their F1 hybrids.

(CBA X M523)F1, (A X M523)F1 and M523 lymphocytes grafted into lethally irradiated CBA or A mice temporarily lose their capacity to respond to test antigens (SRBC, Vi-antigen, S. typhi). Immunoresponsiveness of F1 cells is affected to a lesser degree in lethally irradiated M523 mice. Depression of response is absent in the CBA leads to F1 combination, in the syngeneic combination and in CBA mice whch have received transplanted cells from F1 hybrids which do not share the M523 mutation. The number of hemopoietic (CBA X M523)F1 colonies was also reduced in CBA mice. Resistance of CBA mice to lymphoid (CBA X M523)F1 cells develops 18 days after birth. It can be reduced by additional recipient preirradiation or preinoculation with (CBA X M523)F1 spleen cells. The abrogated resistance can be partially restored by CBA spleen cells. The activity of (CBA X M523)F1 lymphocytes passaged through CBA spleen is restored in syngeneic F1 secondary recipients but inhibited again in the CBA secondary recipients. These results are consistent with the suggestion that resistance of lethally irradiated CBA mice to hemopoietic and lymphoid (CBA X M523)F1 cells is mediated by immunologically competent, radioresistant recipient cells rapidly reacting to transplantation antigens coded by the mutant H-2Kka allele. These cells temporarily suppress the functional activity of transplanted cells but do not eliminate them.

Animals↗
PubMed1989

Therapeutic efficacy of human recombinant interleukin-2 (TGP-3) alone or in combination with cyclophosphamide and immunocompetent cells in allogeneic, semi-syngeneic, and syngeneic murine tumors.

The potential for a recombinant human interleukin-2 (rIL-2, TGP-3) alone, in combination with cyclophosphamide, and in combination with cyclophosphamide and normal immunocompetent cells to manifest biological activity in vivo was tested using allogeneic, semi-syngeneic, and syngeneic tumor-host systems in mice. The biological activity of rIL-2 was evaluated by the inhibition of the growth of tumors and the inhibition of metastases in short-term assays and, in long-term assays, the prolongation of the survival time of mice bearing subcutaneously (s.c.) or intradermally transplanted tumors. rIL-2 was injected s.c. daily continuously for up to 40 days or intermittently two to four times into mice bearing established tumors. In the short-term assays, the dose and schedule dependence of activity of rIL-2 alone was significantly manifested against sarcoma 180 in ICR mice (allogeneic) by the regression of the tumor, and was confirmed against Meth-A fibrosarcoma in BALB/c mice (syngeneic) by retarding the growth of the tumor. When assessed using these tumor, it was found that the antitumor activity of rIL-2 was schedule-dependent: the growth of tumors was more significantly suppressed when rIL-2 was injected every day for 10 days, starting on the 7th day after tumor transplantation, than when rIL-2 was injected five times every other day or twice every 5th day, even if the total amounts of rIL-2 injected were same. The continuous injection for 10 days was considered to be a standard regimen and the daily effective doses of rIL-2 were 5, 10, and 25 micrograms/mouse. Using the standard regimen and the effective doses, the activity of rIL-2 alone was also observed against two other syngeneic tumors: Colon carcinoma 26 in BALB/c mice, by retarding the growth of the tumor, and Lewis lung carcinoma in C57BL/6 mice by reducing the formation of lung metastases. When assessed using M5076 reticulum cell sarcoma, in a long-term assay, the activity of rIL-2 alone was not manifested in C57BL/6 mice (syngeneic) even when rIL-2 was injected for a long period (20 days) but it was observed in BDF1 (semi-syngeneic) mice. On the other hand, it was found that rIL-2 was effective in combination with cyclophosphamide in prolonging the survival time of C57BL/6 mice bearing the tumor.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Cellular interaction against autologous tumor cells between IL-2-cultured lymphocytes and fresh peripheral blood lymphocytes in patients with breast cancer given immuno-chemotherapy.

In patients with Stage II or III breast cancer and in patients with liver metastases from breast cancer, we examined cellular interaction in the cytotoxicity against autologous tumor cells by interleukin-2(IL-2)-cultured lymphocytes (CL) and fresh peripheral blood lymphocytes (FPBL) treated with immunochemotherapy including OK-432 and cyclophosphamide. In flow cytometric analysis, CD8+CD11b+ and CD16+ cells significantly decreased after immuno-chemotherapy in both groups of patients. A protocol study in Stage II or III breast cancer patients showed suppressive activity of FPBL on the cytotoxic activity of CL in 3/9 of the non-treatment group but no suppressive activity and enhancing activity in 3/7 in the immuno-chemotherapy group. Moreover, in 19 patients with liver metastases from breast cancer treated with immuno-chemotherapy including adoptive immunotherapy, FPBL in 6/19 showed enhancing activity, and in 8/19 suppressive activity in the lysis of autologous tumor cells. In assays in vitro using autologous and allogeneic tumor cells, FPBL showed a partial specificity in cellular interaction against autologous tumor cells. CD4-depleted FPBL inhibited cytotoxicity of CL, while CD8-depleted FPBL enhanced cytotoxicity of CL in patients with liver metastases. These results suggest that immuno-chemotherapy eliminates the suppressive population in FPBL and may induce tumor regression if combined with adoptive immunotherapy using CL.

Adjuvants, Immunologic↗
PubMed1985

Involvement of lymphocytes in non-immune inflammation: dual effect of glucocorticoids.

Leucopenia induced by the administration of methotrexate reduced the volume of inflammatory exudate and the number of cells entering the pleural cavity during a 4-h carrageenin pleurisy when compared with that of non-leucopenic controls. The depressed response was partially but markedly restored when leucopenic animals were intravenously injected, immediately before the initiation of pleurisy, with spleen lymphocytes (or their products) obtained from normal, adrenal-demedullated or mock-operated rats. In contrast spleen lymphocytes (or their products) obtained from adrenalectomized rats or from rats receiving metyrapone, an inhibitor of adrenal glucocorticoid biosynthesis, were completely inactive. It is concluded that in physiologic concentrations glucocorticoids are essential for the production of lymphocyte-derived factors involved in the development of acute, non-immune inflammation. In pharmacologic concentrations, however, glucocorticoids suppress the release of such pro-inflammatory factors.

Adrenal Medulla↗
PubMed1992

Maternal immunization by husband's leukocytes for repeated fetal death associated with mild pre-eclampsia--case report with successful outcome.

We report a case of repeated fetal death at 31 gestational weeks associated with mild non-proteinuric pre-eclampsia and intrauterine growth retardation. After double intradermal immunisation with paternal leukocytes, a third pregnancy proceeded uneventfully until it ended at 38 weeks. Maternal anti-paternal blocking antibody activity was assessed by the erythrocyte antibody inhibition (EAI) test. Serologic testing revealed that the couple did not share HLA class I antigens. The mechanisms underlying the likely benefit from immunotherapy are discussed.

Antibody Formation↗