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At least 577 records · Page 32Linked to original sources
PubMed1988

Changes in cellular immunity and nutritional status in mice after thermal injury.

A 13 per cent body surface area (BSA), full skin thickness burn was inflicted on LACA male mice and the changes in cellular immunity and nutritional status were observed. The results showed that thymus, spleen and circulating lymphocytes were significantly involved. A diminished mitogen responsiveness of spleen cells and altered peritoneal macrophage function were confirmed. Ear swelling tests indicated that the cellular immunity of burned mice was most severely depressed in week 2 postburn. The present study also showed that the dramatic change in nutritional status occurred earlier than that in cellular immunity and suggested the importance of early nutritional support after thermal injury.

Animals↗
PubMed1977

Cellular immunity to toxoplasma and besnoitia in hamsters: specificity and the effects of cortisol.

The inhibitory effects of cortisol on cellular immunity were studied in vitro by using hamster peritoneal exudate cells. Two obligate, intracellular protozoa--Toxoplasma gondii and Besnoitia jellisoni-- were used to control for specificity of effects. Results indicate that immune lymphocytes specifically confer immunity to (or "arm") macrophages that specifically express immunity. This arming can be inhibited by 5 microng of cortisol per ml. Macrophages that have been armed already will continue to express immunity (by limiting parasite growth specifically) in the presence of 5 microng of cortisol per ml. Cortisol levels of 20 microng/ml are required to inhibit the expression of immunity by armed macrophages. It was also found that lymphocytes, from hamsters given 20 mg of cortisol subcutaneously 2 days before the harvest of cells, did not arm macrophages, whereas macrophages from these same animals could be armed by immune lymphocytes from untreated hamsters. Therefore, it was concluded that in relation to cellular immunity, lymphocytes are more sensitive to cortisol than are macrophages. Since antibody to these parasites is almost always present in vivo, we also tested the effects of cortisol on the disposition of antibody-modified organisms by activated (not armed) macrophages, and found that 50 microng of cortisol per ml was needed to inhibit macrophage effects on antibody-treated organisms.

Animals↗
PubMed1989

Prenatal diazepam induced persisting depression of cellular immune responses.

Treatment of pregnant Long Evans rats with a low dose of diazepam (1.25 mg/kg per day s.c.) from gestational day (GD) 14 to 20 resulted in severe and long lasting depression of cellular immune responses in male and female offspring. T lymphocyte proliferation, induced by allogeneic stimulation in mixed lymphocyte culture (MLC) or geneic stimulation in mixed lymphocyte culture (MLC) or mitogenic stimulation (concanavalin A), decreased by 50 % or more over a postnatal period of about 2 months. Treatment of the pregnant dam during the early fetal period, from GD 12 to GD 16, did not significantly affect these immune parameters, whereas treatment during later gestation, from GD 16 to 20, significantly affected T lymphocyte function. Clonazepam, a benzodiazepine with high affinity for the central type benzodiazepine site, also affected cellular immune response in offspring. Our data indicate that benzodiazepine treatment during the fetal period may result in persistent postnatal deficiency of cellular immune responses. The relative role of central and peripheral type benzodiazepine receptor and possible interactions with maternal and fetal pituitary - adrenocortical systems are discussed.

Animals↗
PubMed1985

The use of urethane sponge matrix to assess in vivo recovery of murine cellular immunity following syngeneic bone marrow transplantation.

A unique method for assessing the in vivo recovery of cellular immunity following sublethal irradiation and syngeneic bone marrow transplantation of CBA/J mice is described. This method employs the serial surgical implantation of a urethane sponge matrix followed by impregnation of the sponge matrix with alloantigen. Sponge matrices were harvested from each mouse subject at 2 weeks, 4 weeks, and 8 weeks post transplant with and without treatment with interleukin-2. Recovery of cellular immunity was assessed as a function of cytotoxic T lymphocyte activity via cell-mediated lympholysis using chromium labeled targets. Repetitive procedures of implantation and removal of the matrices from the same animal were surgically feasible and were exceptionally well tolerated by the animals with insignificant morbidity thereby permitting continuous monitoring of immunologic recovery. Although the results of treatment with interleukin-2 were inconclusive, this method provides a sensitive, technically manageable means by which to assess an antigenic response in vivo at predetermined time intervals utilizing the same mouse subject. The method additionally affords the potential of being applicable to the in vivo assessment and manipulation of other aspects of the immune response.

Animals↗
PubMed1990

Cellular immunity in pregnant and non-pregnant women with malarial infection.

A study of lymphocyte subpopulation and leucocyte migration inhibition index (LMI) in 78 pregnant and 22 nonpregnant women with malarial infection (P. vivax 60% and P. falciparum 40%) was done in a hospital in Northern India. Eighty pregnant and 20 nonpregnant women without any infection were also included in the study as controls. T-cell percentage in controls decreased to its lowest in first trimester and gradually rose to nonpregnant levels by the end of puerperium. With malarial infection, there was further drop in T-cell percentage, more so in third trimester. LMI in controls corresponded with T-cell percentage and was depressed in pregnant patients. Enhancement in LMI with malarial infection was depressed in pregnant patients maximally in the third trimester. Parity did not have any influence on these cellular immune parameters. Thus, cellular immunity status in malarial patients was found to be depressed during pregnancy especially in the third trimester.

Adolescent↗
PubMedDate not supplied

Cellular immune response in atypical tuberculosis diagnosed by PCR in paraffin embedded material.

The aim was to evaluate the cellular immune response in atypical tuberculosis and granulomatous inflammation consistent with tuberculosis (TBC), negative histochemically for acid-fast bacilli and analysed by PCR for Mycobacterium tuberculosis (MT) detection in paraffin-embedded tissue. Thirty six samples of differently localized atypical tuberculous lesions and granulomatous tuberculoid lesions negative for acid fast bacilli and 4 positive cases on Ziehl-Nielsen stain were analysed by PCR for MT detection and were tested immunohistochemically (IHC) for the cellular immune response in the granulomas and perigranulomatous tissue. The samples selected were: 7 pulmonary and 33 extrapulmonary specimens, especially lymph nodes. Histologically, the atypical tuberculous lesions contained supurative necrosis, defective granulomas and cellular polymorphism. The epithelioid cells showed frequent mitoses. The immunoprofile of cells was polymorphous. L26 positive small lymphocytes were found in nodular lymphoid aggregates surrounding granulomas. A significantly increased number of positive UCHL1 cells were found in 33 out of the 40 analysed cases, with a larger percentage of CD4 positive T cells (81.8% of cases). CD44 was positive in multinucleated giant cells (17.5% of cases), epithelioid cells (60% of cases) and lymphocytes (30% of cases). CD68 was localized in multinucleated giant cells and epithelioid cells, in a 4%, respectively 62.5% of cases. The PCR was performed in all 40 cases; the tissue samples were heterogeneous (lung, lymph nodes, lever, nasopharynx, etc.) and needed a good quality extraction of DNA. Performing a control PCR for Beta Globin tested the extraction; a good result was obtained in 31 cases (77.5%); from these, 19 cases had amplification for IS 6110. The cellular immune response in the atypical tuberculous lesions was similar in cases with and without acid-fast bacilli, but positive for PCR. In the most cases with negative PCR reaction, it was due to a deficient fixation of the material. The T lymphocytes were numerous in all types of tuberculous granulomas, with the prominence of CD4 positive subtype. The immunoprofile of the epithelioid cells, positive for CD44 and CD68, presenting frequently mitoses suggests an activate state in a possible relationship to the T-cell-mediated immune response in tuberculosis.

Antigens, CD↗
PubMed1989

Cellular immune response in Echinococcus multilocularis infection in humans. I. Lymphocyte reactivity to Echinococcus antigens in patients with alveolar echinococcosis.

The involvement of cellular immunity in alveolar echinococcosis (AE) due to E. multilocularis is strongly suggested by the intense granulomatous infiltration observed around the hepatic parasitic lesions, and a progressive decrease of specific cellular immunity has been described in murine AE. However, specific cellular immunity against E. multilocularis has never been documented in human AE. The reactivity to phytohaemagglutinin (PHA) and E. multilocularis antigens of peripheral blood mononuclear cells (PBMC) from 48 patients with AE and 35 control subjects was evaluated by incorporation of 3H-methylthymidine into DNA. A sequential measurement of the proliferative response of PBMC was performed in 20 patients 2 years later, and again in five of them 4 years after the first determination. After stimulation by PHA, the mean proliferation index (PI) of the patients with AE was somewhat higher than that observed in the uninfected controls, but the difference was not significant. The PI obtained with E. multilocularis antigens was higher than the threshold value in all the patients but one, and in five control subjects. The difference between the PI values in the patients with AE and those obtained in the control subjects was highly significant. There was no correlation between the lymphocyte proliferation indices and the specific antibodies assessed using the Em 2-ELISA, or the volume of the parasitic lesions. All the five 'positive' control subjects were living in areas endemic for AE. A previous contract of these subjects with E. multilocularis in the past, followed by a spontaneous elimination of the parasite is possible. The long-term persistence of lymphocyte reactivity to parasite antigens was emphasized by the results of the follow-up of 20 patients with AE: reactivity of PBMC decreased progressively but persisted more than 4 years after complete resection of the parasitic lesions in the patients who underwent a radical surgical procedure. Conversely, an increase in the PI was shown to be usually associated with a progression of the liver lesions.

Adult↗
PubMed2003

[Effect of activation of cellular immunity on p58+ cells expressing killer-cell-inhibitory receptor cells].

UNLABELLED: The purpose of this study was to evaluate the effects of cellular immunity activation on P58(+) cells expressing killer cell inhibitory receptor (KIR) and their regulatory function on cellular immunity, and provid theoretical data for preventing graft-vers-host disease (GVHD) in stem cell transplantation therapy. The mononuclear cells from human peripheral blood were incubated with IL-2, Con A and Lipostin (LP) for 72 hours. The KIR expressing cells, P58.1(+) and P58.2(+) cells, were analyzed by flow cytometry. The results showed that the percentages of CD3(+), CD4(+), CD8(+), CD16(+)CD56(+), P58.1(+) and P58.2(+) cells were greatly increased after treated with IL-2, Con A and LP, separately or in combination, and the percentages of above cells in combined treatment groups were higher than those of single stimulated groups, especially the percentage of cells in the IL-2 + LP group was significantly higher than those in IL-2 and LP singly treated groups. IN CONCLUSION: IL-2, Con A and LP possess the ability to induce the expression of KIR and stimulate proliferation of P58.1(+) and P58.2(+) cells while to activate the celluar immunity response, the expression of P58 gene may be regulated by the activation of cellular immunity.

Adult↗
PubMed1983

[Cellular immunity in idiopathic nephrotic syndrome with minimal glomerular lesions and focal and segmental hyalinosis in children].

Cellular immunity was studied in 31 children presenting with idiopathic nephrotic syndrome (INS), of which 23 with minimal supposed or proven glomerular changes (MGC) and 8 with focal and segmental hyalinosis (FSH). In vivo, a clear hyporeactivity to the delayed hypersensitivity tests and decreased blood T lymphocytes, with a great dispersion of the values were found. Furthermore, such patients' sera display a factor inhibiting the proliferative response of the lymphocytes of patients and of control subjects, to non specific mitogens (PHA), both during exacerbation and remission periods. The hypotheses of an abnormality of cellular immunity and of the existence of an inhibitory factor in the serum of INS with MGC and FSH are discussed.

Adolescent↗
PubMed1977

The relationship of cellular immunity to prognosis in acute leukemia.

Forty-five patients with acute leukemia were compared on cellular immunity measures versus prognosis. The patients were treated according a multicombination therapy protocol. The purified protein derivative (PPD) test and dinitrochlorobenzene (DNCB) test on admission indicated low positive percentages. In acute non-lymphocytic leukemia (ANLL) patients, the 50% survival durations were 11 months in the PPD positive group and 6 months in the PPD negative group. In acute lymphocytic leukemia (ALL) patients, the 50% survival durations were 21 months in the PPD positive group and 13 months in the PPD negative group. Peripheral lymphocyte blastogenesis by phytohemagglutinin (PHA) stimulation was examined at various clinical stages. The stimulation indices were generally low, and no correlation was found between the PHA test and clinical stages. These cellular immunity measures appeared to reflect one aspect of the clinical condition in acute leukemia patients, and further studies are needed for predicting prognosis.

Acute Disease↗
PubMed1980

[Cellular immunity in human brain tumours (author's transl)].

44 patients with various intracranial tumours were examined for cellular immunity to their autologous tumours by the Leucocyte Migration Inhibition Technique (LMI) and by intracutaneous testing. A good correspondence was found in the two tests but LMI seemed to be the more sensitive method. Cellular immunity was found in 3 out of 18 patients with malignant gliomas, in 6 of 16 cases with slower growing gliomas, in 5 of 6 patients with brain sarcoma and in 1 out of 4 patients with meningioma.

Brain Neoplasms↗
PubMedDate not supplied

Metoclopramide and cellular immune functions during polymicrobial sepsis.

Metoclopramide (MCP) has been demonstrated to restore the depressed cellular immune function after hemorrhage by increasing the release of the immunomodulatory pituitary hormone prolactin. We investigated the effect of MCP on serum prolactin concentrations, on cellular immune functions (immune cell distribution, splenocyte proliferation, apoptosis and cytokine release) and on the survival 48 h after induction of a polymicrobial sepsis in mice. Administration of MCP increased circulating serum prolactin concentrations and splenocyte apoptosis rate and improved cellular cytokine release, but did not affect mortality of septic mice. We therefore conclude that administration of MCP modulated splenocyte apoptosis and cytokine release in a murine model of sepsis without an impact on the survival. Furthermore, this effect may be mediated by an increased endogenous prolactin release.

Animals↗
PubMed2005

Effects of fluoxetine on cellular immune response in stressed mice.

We studied the effects of fluoxetine, a non-tricyclic antidepressant drug that selectively inhibits re-uptake of serotonin by presinaptic neurons in the brain, on cellular immune responses in mice exposed to a chronic auditory stressor. The natural killer (NK) cell activity was reduced after 4, 8, 12, 16 and 20 days of stress exposure with a partial recovery on days 16 and 20. Daily treatment with fluoxetine partially reversed these adverse effects of stress in a dose-dependent manner. Significant differences appeared when fluoxetine was administered at 2 mg/kg and maximum effect was reached at doses of 5 mg/kg. The capacity of T cells to generate cytotoxic T-lymphocytes (CTL) in mixed lymphocyte cultures and in vivo was reduced after 4 days of stress application and this effect was partially reduced when mice were injected with 5 mg/kg of fluoxetine. Nevertheless, in our experiments, fluoxetine did not significantly affect the cellular immunity in unstressed mice. In conclusion, fluoxetine seems to partially recover the adverse effects of chronic stress on cellular immune response.

Acoustic Stimulation↗