SEARCH · PubMed Health
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.
Grove et al of Australia studied humoral and cellular immunity in 91 asthmatic patients and found that 18% failed to have an adequate humoral response to a booster dose of tetanus and 9% failed to react to five delayed type hypersensitivity testing antigens. The authors, Gaillard and Larkin, were unable to corroborate these results in their office.
The purpose of this study was to analyze the cellular immune response of women with recurrent spontaneous abortion (RSA) of unknown etiology. The study group was consisted of 117 nonpregnant women with RSA and 44 healthy, nonpregnant multigravidas (as a control). The following immunological parameters were analyzed in peripheral blood of two groups of women: percentage of CD3+, CD4+, CD8+, CD3+/HLA-DR+ and CD16+/CD56+ cells, lymphocyte proliferative response to mitogen and allogenic, and chemiluminescence of neutrophils. The results show that nonpregnant women with RSA of unknown etiology differ in some parameters of immune response form controls. The changes of peripherial blood T lymphocytes subpopulation were observed, consisted on lower CD8+ percentage and higher CD4+ to CD8+ T cells ratio, but lymphocytes and neutrophils activity seems to be unchanged. It seems, that among couples experiencing RSA of unknown etiology higher evidence of the same HLA antigents is not observed, when compared with couples of normal fertility.
BACKGROUND: Cancer patients have often been reported to have impaired immune function, and the effect of treatment modalities, such as surgery, irradiation, and chemotherapy, in depressing patients' immunity has also been reported. In this investigation, the effect of treatment on the cellular immunity of esophageal cancer patients was evaluated. METHODS: Immunological parameters, such as natural killer (NK) activity and lymphocyte subsets in peripheral blood, were measured in 32 esophageal cancer patients on 5 occasions (on the day of admission, 2 days before surgery, and 1 week, 1 month, and 2 months after surgery). RESULTS: NK activity was greatly impaired shortly after the operation, and the percentages of lymphocytes as a whole, and CD8+, CD16+, and CD57+ lymphocytes were significantly decreased, on the other hand, a postoperative increase in the CD4+/CD8+ ratio was observed. No significant depression of immune function by postoperative irradiation was observed. CONCLUSIONS: The results of this study suggest that cellular immunity, especially cytotoxicity, shortly after esophagectomy may be greatly impaired by the surgical stress of esophagectomy and an added effect of chemotherapy.
Cellular immunity to herpes simplex virus type 1 (HSV-1) in 12 volunteers with recurrent herpes labialis was evaluated by means of two microassays. In the blastogenesis assay, lymphocytes were incubated with tissue culture cells persistently infected with HSV-1. Uninfected cells were used as controls, and a blastogenic index was calculated. The mean blastogenic index (plus or minus SD) for subjects with recurrent herpes labialis was 26.9 (plus or minus 8.3); the mean blastogenic index (plus or minus SD) in control donors with antibody to HSV-1 was 13.4 (plus or minus 7.2). The difference between these values was statistically significant (t equals 4.154; P smaller than 0.001). In the cytotoxicity assay, cells of the same persistently infected line were used as target cells, and release of 51-Cr from these cells or from control cells served as the index of lymphocyte reactivity. Specific immune release attributable to HSV-1 averages 3.7% (plus or minus 1.8%) in subjects with recurrent herpes labialis, compared with 23.1% (plus or minus 9.8%) in controls (t equals 6.135; P smaller than 0.001). These data suggest a dissociation between mechanisms of cellular immunity, with enhanced lymphocyte blastogenesis but decreased cytotoxicity. Recurrent herpes labialis may thus result from subtle cellular immune deficiency involving at least one of the efferent mechanisms.
The micromethod of leukocyte migration inhibition test was used to study cellular immunity in patients with multiple sclerosis (MS) to measles virus antigens and some other infectious (vaccinia virus, tuberculin) and noninfectious (brain white matter extract) antigens. In MS patients the reaction to measles antigen was weaker than in the control group, while the reactivity to the brain white matter extract was increased. As for the responses to vaccinia virus and tuberculin, these two grous did not differ statistically. The population of MS patients under study was not homogeneous in the intensity of measles cellular immunity (MCI). In the early stages of multiple sclerosis, MCI indices did not differ from those in the control group. MCI was the weakest in those subjects developing MS early in life who showed rapid worsening of the clinical status. Besides, MCI values were age-related: in older age groups they were low both in MS patients and in control subjects.
Experimental evidence from previous studies supports the conclusion that orally administered lactoferrin (LF) restores the immune response in mice treated with a sublethal dose of cyclophosphamide (CP). The aim of this study was to elucidate potential benefit of LF in mice undergoing chemotherapy with busulfan (BU) and CP, followed by intravenous (i.v.) injection of bone marrow cells. CBA mice were treated orally with busulfan (4 mg/kg) for 4 consecutive days, followed by two daily doses of CP delivered intraperitoneally (i.p.) at a dose of 100 mg/kg and reconstituted next day with i.v. injection of 10(7) syngeneic bone marrow cells. One group of these mice was given LF in drinking water (0.5% solution). After treatment, mice were immunized with ovalbumin (OVA) to subsequently measure delayed type hypersensitivity responsiveness and with sheep red blood cells to determine humoral immunity by evaluation of splenic antibody-forming cells. As expected, both humoral and cellular immune responses of mice that were treated with these chemotherapeutic agents was markedly impaired. Here we report that this impairment was remarkably attenuated by oral administration of LF. Humoral immunity fell to levels that were 66-88% lower than that of untreated animals. Humoral immunity of LF-treated animals was equivalent to that of untreated mice within 1 month. Cellular immune responses were inhibited by chemotherapy treatment to a lesser degree, reaching levels that were approximately 50% lower than those of untreated animals. Again, LF mitigated this decrease, resulting in responses that were only slightly lower than those observed in untreated animals. Furthermore, when mice were given a lethal dose of BU (4 x 25 mg daily doses, i.p.) followed by a bone marrow transplant, LF caused enhanced lympho-, erythro-, and myelopoiesis in the bone marrow and appearance of transforming splenic lymphoblasts, similar to effects caused by administration of recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF). In summary, our study suggests that LF may be a useful agent to accelerate restoration of immune responsiveness induced by chemotherapy in bone marrow transplant recipients.
We have investigated the effect of exposure to ozone on defense mechanisms to a respiratory infection with Listeria monocytogenes in the rat. For this purpose rats were continuously exposed to O3 concentrations ranging from 0.25 to 2.0 mg/m3 for a period of 1 week. In this model defense to a respiratory infection with Listeria depends on acquired specific cellular immune responses, as well as on natural nonspecific defense mechanisms. The results confirm earlier findings that show that ozone exposure can suppress the capacity of macrophages to ingest and kill Listeria. Moreover, the results show that ozone can also have a suppressive effect on the development of cellular immune responses to a respiratory Listeria infection, i.e., on T/B ratios in lung draining lymph nodes, delayed-type hypersensitivity responses to Listeria antigen, and lymphoproliferative responses in spleen and lung draining lymph nodes to Listeria antigen. The effects on the specific immune responses are especially overt if exposure to the oxidant gas occurs during an ongoing primary infection. The pathological lesions induced by a pulmonary Listeria monocytogenes infection were characterized by multifocal infiltrates of histiocytic and lymphoid cells. The foci sometimes had a granulomatous appearance. Moreover, the cellularity of the interstitial tissues was increased. In the lung many diffuse alveolar macrophages could be seen in the alveoli. Ozone exposure greatly increased the severity of the lung lesions and also of liver lesions resulting from the pulmonary infection. A prominent finding was the formation of granulomas in ozone-exposed and Listeria-infected rats. This increased severity of the lesions after ozone exposure and subsequent infection with Listeria was presumably not a result of additive ozone and Listeria-induced lesions, but rather an effect of ozone-induced impaired clearance of the bacteria, caused by depressed macrophage activity and cellular immunity. T-cell-dependent immune responses form an important component of defense to respiratory infections with bacteria and viruses, and possibly also to neoplasms. Since our study unequivocally shows an effect on T-cell-dependent immunity, ozone exposure has to be judged potentially hazardous with respect to such challenges of the lung.
Enterovirus-specific cellular immunity was studied in Estonian and in Finnish children at the age of 9 months. The aim was to evaluate the level of responsiveness in two neighbouring countries with different poliovirus immunization practices and striking differences in the incidence of insulin-dependent diabetes mellitus (IDDM), a disease in which early enterovirus infections are an aetiological risk factor. The Estonian children immunized with live attenuated polio vaccine had stronger T cell responses to coxsackievirus B4 and poliovirus type 1 when compared with Finnish children immunized with inactivated polio vaccine (median stimulation indices 10.4 and 6.3 in Estonian children and 1.9 and 2.9 in Finnish children, respectively; P < 0.05). Lymphocytes stimulated by poliovirus type 1 antigen expressed interferon-gamma (IFN-gamma) mRNAs, which strongly correlated with the level of proliferation responses. Lymphocytes of Estonian children had a tendency towards stronger expression of IFN-gamma upon poliovirus challenge when compared with Finnish children. The number of children who had experienced coxsackievirus B infections, as determined by the presence of neutralizing antibodies, did not differ between Estonian and Finnish children. The results show that Finnish children have weaker cellular immunity against enteroviruses at the age of 9 months compared with Estonian children at the same age. This is most probably due to the difference in polio vaccination schedules; in Estonia live poliovirus vaccine is used and given at earlier ages than the inactivated vaccines in Finland. This leads to stronger T cell immunity which cross-reacts with other enterovirus serotypes. This may explain the lower incidence of IDDM in Estonia by providing effective protection against diabetogenic enterovirus strains in Estonian children.
AIM: To explore the effects of liniment levamisole on cellular immune functions of patients with chronic hepatitis B. METHODS: The levels of T lymphocyte subsets and mIL-2R in peripheral blood mononuclear cells (PBMCs) were measured by biotin-streptavidin (BSA) technique in patients with chronic hepatitis B before and after the treatment with liniment levamisole. RESULTS: After one course of treatment with liniment levamisole, the levels of CD3(+), CD4(+), and the ratio of CD4(+)/CD8(+) increased as compared to those before the treatment but the level of CD8(+) decreased. The total expression level of mIL-2R in PBMCs increased before and after the treatment with liniment levamisole. CONCLUSION: Liniment levamisole may reinforce cellular immune functions of patients with chronic hepatitis B.
Effects of some imidazole compounds were studied on two animal models of cellular immune responses. Metronidazole in doses of 100 and 200 mg/kg and cimetidine 200mg/kg (ip), significantly suppressed the delayed type of hypersensitivity reaction, as evidenced by the footpad thickness method in mice. No significant alteration in the response could be observed however, in tinidazole treated groups. All the three drugs inhibited the migration of leucocytes in the presence of antigen in rats considerably. However, they did not produce any involution of spleen or reduction of adrenal weight indicating that their actions are not corticosteroid mediated. All the three drugs studied are histamine-like imidazole derivatives. H2 receptors are present on the surface of T-lymphocytes. They appear to modulate the cellular immune response by altering the function of the regulatory lymphocytes.
We analyzed the local and systemic cellular immune response in mongolian gerbils inoculated with Entamoeba histolytica. Two groups were intracecally inoculated with E. histolytica trophozoites and two groups were used as controls. A inoculated groups and a control groups were sacrificed on days 10 and 30 post inoculation (p.i), the spleen and mesenteric lymph nodes (MLNs) lymphocytes (Ly) were isolated and incubated in vitro with 2 different amebic antigens. The proliferative Ly response of inoculated groups was greater than the Ly mitogenic response seen in control groups, at day 10 p.i. as well as day 30 p.i. (alpha = 0.05). Ly response of MLNs was greater in comparison to those of the spleen (alpha = 0.05). In other four groups, intradermal reactions with a antigen were used to demonstrated delayed hypersensitivity in gerbils after being inoculated with E. histolytica trophozoites. The percentage of volume increase of the plantar pad swelling were measured. Groups inoculated presented greater increases (alpha = 0.05) than groups controls. The evidence presented herein demonstrates that the presence of E. histolytica trophozoites in cecum induced a local and systemic cellular immune response.
Mice of the RF/J strain on a normal diet are defective in some aspects of cellular immunity, as evidenced by their susceptibility to infection with Candida albicans, their failure to release detectable quantities of circulating migration inhibitory factor (MIF) in vivo, and the presence of a low rate of phagocytosis and killing by peritoneal macrophages. When the mice were fed a high-zinc diet (300 ppm) for 4 weeks and then treated daily with 160 ng prothymosin alpha, an increase occurred in resistance to infection with C. albicans, in the capacity to release MIF in vivo into the circulation and in the capacity of peritoneal macrophages to engulf (phagocytose) and kill cells of C. krusei. In addition, the number of spleen lymphocytes producing antibody to a T-dependent antigen was significantly increased in the mice fed a high-zinc diet and inoculated daily with prothymosin alpha.
Hemorrhagic shock is associated with increasing catecholamine plasma concentrations. Plasma catecholamines are known to affect cellular immune functions. We therefore, investigated the effect of endogenously released catecholamines on lymphocyte distribution (CD4+ lymphocytes, CD8+ lymphocytes, and natural killer (NK) cells), splenocyte apoptosis (Annexin V binding), tumor necrosis factor-alpha (TNF-alpha), and interleukin 10 (IL-10) release during a volume-controlled hemorrhagic shock in mice. Mice received either saline (HEM), the non-selective beta-adrenoceptor antagonist propranolol (PROP; 2 mg/kg i.p.), or the beta1-adrenoceptor antagonist metoprolol (MET; 2 mg/kg i.p.) before induction of hemorrhage. Mice were sacrificed to obtain the spleen and whole blood 1 h after hemorrhage, 1 h after fluid resuscitation, and 24 h after hemorrhage. Flow cytometric analysis revealed an increase in circulating NK cells in the HEM group. This effect was completely abolished by pretreatment with propranolol or metoprolol. Furthermore, administration of either beta-adrenoceptor antagonist led to a decrease of circulating CD8+ lymphocyte numbers. Monitoring of splenocyte apoptosis by determination of Annexin V binding revealed an increase in splenocyte apoptosis 24 h after hemorrhage in the HEM group but not in the animals pretreated with propranolol or metoprolol. Induction of hemorrhage did not affect TNF-alpha or IL-10 plasma concentrations in either experimental group. We conclude that plasma catecholamines affect cellular immunity in the early phase of trauma via a beta-adrenergic pathway.
This study examined the effects of the widely used immunosuppressor cyclosporine A and of one of its derivatives, cyclosporine G, on glucose tolerance, cellular immunity, and renal and hepatic function, in relation to their pharmacokinetic profile in Wistar rats. After 3 weeks of daily cyclosporine A doses of 10 mg/kg body weight plasma cyclosporine levels were higher in male than in female rats. This was associated in male rats with marked decrease in lymphocyte subsets, affecting particularly the OX19+ T cells, with glucose intolerance, and an increase in plasma creatinine. The female rats had none of these effects. After 3 weeks of daily cyclosporine G doses of 10 mg/kg body weight, plasma cyclosporine levels were higher in male than female animals, and higher than with cyclosporine A in both sexes. Similar cellular immune effects and glucose intolerance were seen in male rats, but of a lesser magnitude than with cyclosporine A. No increase in creatinine was seen, but rats of both sexes treated with cyclosporine G had elevated plasma bilirubin. We conclude that (1) both cyclosporine A and G can cause glucose intolerance, (2) the cyclosporine plasma levels are higher in male than in female rats and with cyclosporine G than with cyclosporine A, for the same oral dose, (3) the absence of glucose intolerance, nephrotoxicity, and cellular immune changes in female rats treated with cyclosporine A is related to their lower cyclosporine levels, and (4) cyclosporine G is less nephrotoxic than cyclosporine A, but more hepatotoxic.
Recombinant human immunodeficiency virus type-1 (HIV-1)-like gag-env particles produced in mammalian cells were inoculated into two New Zealand white rabbits. In parallel, two control rabbits were inoculated with the homologous HIV-1 virions inactivated by ultra violet light (uv) and psoralen treatments. The humoral and cellular immune responses to HIV-1 were evaluated for both groups of animals. Recombinant particles elicited humoral immunity that was specific for all the viral structural proteins. The antibodies recognized both denatured and nondenatured proteins. Moreover, the sera neutralized the in vitro infectivity of the homologous virus in CEM cells. Importantly, the recombinant particles also generated a T helper response by priming with the HIV proteins. Similar results were observed with inactivated virus immunization. Therefore, our results suggest that the recombinant HIV-like particles elicit functional humoral immunity as well as cellular immunity and represent a novel vaccine candidate for AIDS.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.