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The cellular immunity of 12 adult subjects suffering from nephro-epithelioma was studied by means of lymphoblastic transformation tests repeated regularly. Perhaps a certain agreement could be observed between the clinical course and the subject's sensitization to the tumor antigens.
A preliminary study was conducted to determine the cellular immune status of neonatal, colostrum-deprived calves following inoculation with either attenuated or virulent bovine coronavirus (BCV). Uninfected calves served as controls. To determine the intestinal and systemic cellular immune status, we performed MHC-restricted cytotoxic lymphocyte (CTL) assay on mesenteric lymphocytes, enumerated T cell subsets in peripheral blood lymphocytes, and examined histopathological alterations in mesenteric lymph nodes and gut-associated lymphoid tissue. Target cells for the CTL assay were autologous testicular cells and effector cells were mesenteric lymphocytes from calves infected with BCV. No appreciable specific lysis was observed in any group of calves indicating the absence of demonstrable CTL responses. The TC/TS population was severely depressed in the calf inoculated with the virulent virus but not in those inoculated with either the attenuated virus or placebo. The mesenteric lymph nodes and Peyer's patches of calves inoculated with the virulent virus showed severe depletion of lymphocytes. These calves developed intestinal antibody responses in the acute phase of infection (1 week after infection) but were immunosuppressed in the later stage of infection.
Enhanced cellular immunity following influenza vaccination has been undetectable in kidney transplant recipients so far. Protection from influenza is dependent on cellular and humoral immunity. Aim of the study was to investigate immune responses before and after vaccination with influenza A and B antigens in 65 kidney transplant recipients. A significant increase in proliferative responses was only observed towards influenza B (P < 0.0001) by lymphocyte transformation test. The enzyme-linked immunospot (ELISpot) assay was more sensitive and detected significant, 3- to 5-fold increases (P < 0.0001) in interferon-gamma secretion using influenza A and B antigens. Furthermore, influenza antibody titers increased significantly (P < 0.0001). At month 1 post-vaccination 85% of patients displayed specific cellular, and 95% or 92% humoral immunity against influenza A and B, respectively. Thus, applying the sensitive ELISpot assay, influenza-specific cellular immunity could be detected for the first time in kidney transplant recipients after vaccination.
There has been a recent rapid increase in the number of assays for cellular immunity in man and in information related to the mechanisms underlying the observed reactions. These tests have been applied clinically for three main purposes: (a) Evaluation of cell-mediated immune competence of patients with primary immune deficiencies and of possible immunological depression associated with cancer or other diseases. (b) Determination of major differences in histocompatibility antigens which might be important in rejection of organ transplants. Some cellular immune assays have become part of the routine battery of assays used for immunological evaluation of potential donors and recipients. (c) Measurement of specific immune reactivity against antigens associated with a variety of diseases, including infectious diseases, autoimmune diseases and cancer.
Intracutaneous immunization of BALB/c mice with purified inactivated Semliki Forest virus resulted in cellular immunity without detectable antibodies. The animals were protected against subcutaneous challenge, from which the challenge virus spreads slowly. After intraperitoneal challenge, which permits a rapid virus spread, the protection was marginal. Stimulation of the intraperitoneal cell population with thioglycolate before challenge resulted in complete protection. The protection could be transferred to normal mice with peripheral lymph node cells, but not with spleen cells. The course of the infection in immunized and normal mice was also studied. Semliki Forest virus does not multiply in peritoneal cells in vivo. In immunized mice part of the challenge virus in the peritoneal cavity was rapidly eliminated and viremia was reduced. After challenge, immunized mice produced less antibody than normal mice.
Three males with the X-linked lymphoproliferative syndrome (XLP) with hypo- or agammaglobulinemia following Epstein-Barr virus (EBV) infection and two males with the chronic mononucleosis syndrome were investigated for immune responses to EBV-determined antigens. Males with XLP showed profound cellular immune defects. Markedly diminished responses of natural killer cell and interferon-activated killer cell activities and impaired leukocyte migration inhibition responses to phytohemagglutinin were determined in patients with XLP. The two patients with chronic mononucleosis showed less severe defects. All patients showed partial or complete impairment of their EBV-specific immune responses as measured by leukocyte migration inhibition. EBV-specific antibodies were markedly diminished against EBV-associated nuclear antigen, early antigen, and viral capsid antigen in males with XLP. In contrast, patients with chronic mononucleosis had elevated antibodies to most EBV-specific antigens. Individuals with life-threatening EBV-induced lymphoproliferative disorders may exhibit multiple defective immune mechanisms against the virus.
OBJECTIVE: Local cellular immune response and traditional histopathologic parameters in endometrial carcinoma patients 50 years old and younger were compared with those of patients older than 50 years of age. MATERIALS AND METHODS: We retrospectively compared the clinicopathologic factors and outcomes of 24 younger and 82 older women who were operated on for endometrioid type endometrial carcinoma at our institution. RESULTS: No significant difference was determined in survival with respect to age and menopausal status in patients with endometrial carcinoma. Younger and older age groups had a similar distribution of most pathologic features including myometrial invasion, cervical involvement, lymph node metastasis, vascular invasion, perivascular lymphocytic infiltrates and tumor infiltrating lymphocytes. While older women had higher-grade tumors, younger women had more frequent ovarian metastasis. Tumor infilrating lymphocytes were seen more frequently in the postmenopausal group than those of the premenopausal group. CONCLUSION: The distribution of local cellular immune response, most histopathologic parameters and survival were the same for younger and older women.
Peripheral cellular immunity of ten dogs with keratoconjunctivitis sicca (KCS) that had not been treated with topical corticosteroids or cyclosporine was evaluated (by use of in vitro lymphocyte proliferation assays and CD4+/CD8+ lymphocyte subset analysis) before and after 1 and 3 months of treatment with topical ocular 2% cyclosporine (CsA). In vitro lymphocyte proliferation and CD4+/CD8+ lymphocyte subset analysis was done in eight normal dogs at the 0, 1 and 3 month time periods to use for comparison. There was no significant difference in lymphocyte proliferation or numbers of CD4+ or CD8+ lymphocytes in dogs with KCS and normal dogs prior to CsA treatment. However, by 1 month's time, lymphocyte proliferation had decreased in the CsA-treated Dogs with KCS, and by 3 months there was a significant difference (P < 0.0001) from the normal dogs. These results suggest that dogs with KCS may not have altered peripheral cellular immunity and that use of topical 2% cyclosporine for treatment of KCS causes a suppression of lymphocyte proliferation after 1 to 3 months of use.
Over the past few years, major advances in several areas of immunology have provided a foundation for the rational design of vaccines against diseases requiring cellular immunity. Among these advances are the cellular mechanisms by which DNA vaccines can sustain long-term humoral and cellular immunity.
Ethanol was found to alter functioning and numbers of lymphoid cells of the cellular immune system in humans and rats. In in-vitro studies on human lymphocytes, a higher than 0.1% concentration of ethanol and acetaldehyde and acetic acid, the metabolites of ethanol, caused a decrease in the formation of E-rosettes. Methanol and propanol also resulted in a decrease in E-rosette formation. The natural killer (NK) cells varied in their ability to lyse tumor cells. In vitro, the NK-cell activity declined at higher than 0.2% concentration of ethanol. The NK activity in cells isolated from spleen and thymus of rats fed 1 g/dl or 7 g/dl ethanol did not differ significantly from the controls. Sprague Dawley rats fed 1 g/dl or 7 g/dl ethanol for 12 weeks had a significantly smaller thymus compared to the controls. Alveolar macrophages isolated from the rats exhibited impaired phagocytic activity. In agreement with other investigators, ethanol was found to result in a loss of T-cell population in the spleens of rats fed ethanol for 13 months. On the other hand, the T-helper cells and the proportion of T-helper to T-suppressor cells were found to increase in the splenocytes from these rats. This latter occurrence, apparently, is to compensate for the general loss of T-cell population observed in the body that occurs with ethanol ingestion. It is hypothesized that immunosuppression and the transient imbalances in the components of the cellular immunity induced by ethanol lead to an increased risk of pathogenesis associated with alcohol consumption.
The effects of zinc and/or melatonin deficiencies on cellular immunity were investigated in rats infected with Toxoplasma gondii. A total of 50 adult male Sprague-Dawley rats were divided into 5 groups of 10 rats each. In group I, the rats were infected with T. gondii and fed a zinc-deficient diet; in group II, the rats were infected and their pineal gland was surgically removed. Group III included rats that were infected, pinealectomized, and fed a zinc-deficient diet. Group IV consisted of T. gondii-infested rats that received no treatment of any kind, and group V were normal controls. After 3 wk of treatment, all rats were sacrificed and the percentages of CD3, CD4, and CD8 lymphocytes, zinc, and melatonin levels in plasma and the percentage of lymphocyte in blood smears were analyzed. The CD3 ratios of groups I-III were significantly lower than those of groups IV and V (p<0.01). The CD4 lymphocytes were significantly higher in group IV than that in all other groups (p<0.05). In group IV, the CD8 lymphocytes were higher than in groups I-III (p<0.01) and those in group V were higher than for groups I and III (p<0.01). Lymphocyte incidence in group IV was higher than in the other four groups (p<0.01). The plasma zinc and plasma melatonin levels in groups I-III were significantly lower than those in the controls (p<0.01, both cases). These results suggest that zinc and/or melatonin deficiency have a negative influence on cellular immunity in rats with toxoplasmosis.
An in vitro model of cellular immunity in the guinea pig was established. Animals were immunized with tubercle bacilli, bovine gamma globulin, or picrylated human serum albumin in complete Freund's adjuvant. Oil-induced peritoneal exudates from immune and control animals were cultured overnight with and without specific antigen. The cultures were washed and the macrophage monolayers were infected with Listeria monocytogenes. At intervals the monolayers were lysed and the numbers of viable intracellular bacteria were quantitated by pour plate cultures. Random monolayers were also evaluated in sequence by visually counting the intracellular bacteria on Gram-stained plates. Both methods demonstrated that the macrophages from immune animals had markedly enhanced listericidal activity when the peritoneal exudates were cultured with antigen before infection. Macrophage migration inhibition was also demonstrated under these conditions. The experiments reported here describe an in vitro model of cellular immunity which will allow separation and recombination of cell types and direct assay of cell products in efforts to elucidate further the mechanisms of the immunologically mediated enhancement of macrophage bactericidal capacity.
Typhoid fever is an infectious disease commonly seen in the tropics, with multisystem involvement and a high morbidity and mortality rate. Legionnaires' disease: a newly described acute respiratory infection by unusual aerobic gram-negative micro-organisms namely Legionella pneumophila. Cellular immunity: in vitro and in vivo evaluations of cellular immunity using E-rosette formation (E) and 2.4-Dinitrochlorobenzene (D) reaction were made in typhoid fever, amebiasis and Legionnaires' disease. Results will be presented. Three patients with relapsing typhoid fever were given transfer factor and another group with typhoid fever were given Levamisole with sulfamethoxazole-trimethoprim. Up to 90% of the cases receiving immunopotentiating factors/agents improved faster in both general condition, fever and cellular immunity.
Whether immunity against opportunistic pathogens can be fully restored by control of HIV-1 replication remains open to question. This longitudinal study was conducted to measure anti-tuberculosis (TB) cellular immunity in 13 HIV-1/TB-coinfected patients effectively treated by highly active antiretroviral therapy (HAART) in a period of 12 months. In this study, anti-TB cellular immunity was assessed by determining the frequencies of CD 69 expression on CD4+ and CD8+ T cells in response to purified protein derivative (PPD) stimulation (abbreviated as %CD4+CD69 to PPD and %CD8+CD69 to PPD). Here, we show that %CD4+CD69 to PPD correlated with the results of tuberculin skin tests and interferon-gamma (IFN-gamma) production from PPD-stimulated CD4+ T cells, and %CD8+CD69 to PPD also correlated with CD8+ T cell-mediated PPD-specific cytolysis. In overall analysis for these 13 patients, both %CD4+CD69 to PPD and %CD8+CD69 to PPD increased significantly during the 12 months (p =. 003 and p <.001, respectively). However, we found %CD4+CD69 to PPD or %CD8+CD69 to PPD failed to increase substantially in some patients (i.e., immunologic nonresponders). A significantly higher proportion of patients whose baseline CD4+ count was <50 cells/mm3 were considered to be CD4+ nonresponders compared with those whose baseline CD4+ count was >50 cells/mm3. Furthermore, baseline CD4+ cell count in nonresponders is significantly lower than that in responders, although the effectiveness of HAART did not differ between them. Our results indicate that PPD-specific frequencies of CD69 expression may be used as surrogate markers of anti-TB cellular immunity. By this method, we show that full reconstitution of anti-TB cellular immunity in HIV-1/TB coinfected patients may not necessarily be achieved by "successful" HAART and may be influenced by the baseline immune status when HAART is started. These data suggest that the decision to discontinue secondary prophylaxis for opportunistic infections should be cautiously made, even when the CD4+ cell count has significantly increased.
It is widely accepted that alcohol exposure is a causative factor in the occurrence of burn or other traumatic injury. It is less well known that individuals who have consumed alcohol before sustaining an injury suffer from increased morbidity and mortality compared with the morbidity and mortality of non-alcohol-consuming subjects with similar injuries. Complications due to bacterial infection are the most common burn sequelae in injured patients and are frequently associated with depressed immunity. Independently, alcohol exposure and injury have been shown to influence cellular immunity negatively. These changes in immunity are closely linked to injury- or alcohol-induced alterations in the cytokine milieu in both clinical studies and animal models. Not surprisingly, the combination of insult of alcohol exposure and burn injury results in immune suppression that is greater in magnitude and duration compared with either insult alone. The combined effects of alcohol and injury on immunity have been examined in a limited number of studies. However, results of these studies support the suggestion that altered cytokine production is an integral part of the immune dysregulation and increased mortality that is observed. In particular, the increased presence of macrophage-derived mediators observed after burn or alcohol exposure alone seems to be synergistically increased in a combined injury model. Although more research is needed, it is likely that therapeutic modalities that include manipulation of cytokine networks to boost cellular immunity may improve outcome for patients who sustain injuries subsequent to consuming alcohol.
Autoantibodies to the neuroendocrine protein insulinoma-associated protein 2 (IA-2), a member of the tyrosine phosphatase family, have been observed in individuals with or at increased risk for IDDM. Because this disease is thought to result from a T-cell-mediated autoimmune destruction of the insulin-producing pancreatic beta-cells, we analyzed humoral and cellular immune reactivity to this autoantigen to further define its role in the pathogenesis of IDDM. Peripheral blood mononuclear cells (PBMC) from individuals with newly diagnosed IDDM or at varying levels of risk for the disease were stimulated in vitro with the entire 42-kDa internal domain of IA-2 (amino acids 603-979), a series of control antigens (glutathionine-S-transferase, tetanus toxoid, Candida albicans, mumps, bovine serum albumin), and a mitogen (phytohemagglutinin). The frequency and mean stimulation index of PBMC proliferation against IA-2 was significantly higher in newly diagnosed IDDM subjects (14 of 33 [42%]; 3.8+/-4.5 at 10 microg/ml) and autoantibody-positive relatives at increased risk for IDDM (6 of 9 [66%]; 3.9+/-3.2) compared with autoantibody-negative relatives (1 of 15 [7%]; 1.8+/-1.0) or healthy control subjects (1 of 12 [8%]; 1.5+/-1.0). The frequencies of cellular immune reactivities to all other antigens were remarkably similar between each subject group. Sera from 58% of the newly diagnosed IDDM patients tested were IA-2 autoantibody positive. Despite investigations suggesting an inverse association between humoral and cellular immune reactivities against islet-cell-associated autoantigens, no such relationship was observed (rs=0.18, P=0.39) with respect to IA-2. These studies support the autoantigenic nature of IA-2 in IDDM and suggest the inclusion of cellular immune responses as an adjunct marker for the disease.
Partial DiGeorge syndrome (pDGS) is an inherited primary immunodeficiency syndrome (incidence, 1:3000 live births) primarily affecting cellular immune function; partial, infers thymic hypoplasia with detectable circulating T-lymphocytes and adequate function. No guidelines exist regarding the recommendations for use of live viral vaccines (LVVs) in this extensive population of pediatric patients. We reviewed the experience with live viral vaccines in our cohort of patients with pDGS. Of 53 patients, 25 (47%) had received a live viral vaccine. No significant adverse events were recorded in association with administration of live viral vaccines. There was no statistically significant difference between cellular immune function at initial presentation between those patients that received live viral vaccines and those that did not. Adequate cellular immune function was documented for 15 of the 25 LVV recipients at the time of vaccine administration without significant change from baseline. These observations suggest that live viral vaccines appear safe in patients with pDGS and stable immune function.
Children with kwashiorkor showed a high incidence of deranged cellular immunity as evidenced by impairment of delayed cutaneous hypersensitivity reactions to candida and diphtheria toxoid antigens and of lymphocyte transformation after phytohaemagglutinin stimulation. This may contribute to their susceptibility to infection. A correlation was shown between the degree of impairment of tests of cellular immunity and the severity of the kwashiorkor. Once recovery was initiated the skin tests gave the expected positive results and the lymphocyte transformation index improved. Protein deprivation may result in impaired deoxyribonucleic acid (DNA) synthesis and in atrophy of both the thymus and the lymphoid tissue.