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At least 469 records · Page 26Linked to original sources
PubMed2001

Respiratory virus infections in adult T cell-depleted transplant recipients: the role of cellular immunity.

BACKGROUND: Little is known about the role of cellular immunity in respiratory virus infections after bone marrow transplantation. METHODS: Forty allograft recipients T-cell depleted with Campath antibodies were evaluated for respiratory virus infections in an active surveillance program with early initiation of antiviral therapy. RESULTS: Eighteen episodes of respiratory virus infection were detected in nine patients (22%) at a median of 95 days, with lower respiratory involvement in 44%. Fourteen episodes were treated with antiviral therapy for 7 to 46 days, with 11% mortality. Respiratory virus infections were more common in patients receiving Campath 100 mg in vivo, but delayed CD4+ recovery was the most significant risk factor. CONCLUSIONS: Respiratory virus infections are common and often recurrent in patients with severe CD4+ T lymphopenia. However, the mortality was low, which may have been due to early institution of antiviral treatment or reduced inflammatory damage to the lungs due to severe lymphopenia.

CD4-Positive T-Lymphocytes↗
PubMed1982

Influence of high caloric parenteral nutrition on catabolism and cellular immune competence in carcinoma patients.

Urea production rate and cellular immune reactivity measured by skin stamp test were used to determine the extent of protein catabolism in 30 surgical patients with histologically diagnosed gastrointestinal carcinoma. All patients received high-caloric total parenteral nutrition (TPN) preoperatively. In those patients with an urea production rate of less than 15 g/day (according to definition of non-catabolic state) TPN was discontinued and the operation performed immediately, whereas the remaining 13 patients with an urea production rate exceeding 15 g/day (according to definition a catabolic state) were given TPN a total of 10 days prior to operation. Nine of the 13 patients could be converted from a catabolic to a non-catabolic state. Only one of these patients died, whereas of the remaining 4 patients who - according to the definition - remained in a catabolic state, two died. The course of nutrition positively influenced the serum levels of IgG, IgA and IgM. The skin stamp test was positive in only three of the 13 patients. Obviously, a positive skin test reaction occurred only in those patients who could be returned to a non-catabolic state during the course of TPN. By means of preoperative TPN catabolic patients can be converted into a non-catabolic state which is associated with a reduction in morbidity and mortality. Moreover, high caloric parenteral nutrition rich in amino acids seem to improve the prognosis for patients with negative skin test reactivity.

Amino Acids↗
PubMed1996

Cellular immunity and hypersensitivity as components of periodontal destruction.

BACKGROUND: Cellular immunity has been implicated in periodontal destruction for over 25 years. Studies in the 1970s used lymphocyte transformation and lymphokine assays to establish a role for cell-mediated mechanisms in periodontal disease. Immunohistological studies subsequently showed that the formation of gingivitis followed a similar pattern to the formation of a delayed type hypersensitivity reaction. Further functional studies suggested that a T cell/macrophage immunoregulatory imbalance may exist locally in the periodontitis lesion and that this imbalance may be antigen specific. RECENT EVIDENCE: More recently, T cell subsets have been dichotomised on the basis of their cytokine profiles. In general, ThI cells produce IL-2 and IFN-gamma while Th2 cells produce IL-4, IL-5 and IL-6. The major function of Th1 cells is to mediate delayed type hypersensitivity. In contrast the major function of Th2 cells is to provide B cell help. HYPOTHESIS: A model for periodontal disease has now been developed based on this functional dichotomy which provides a framework for the study of cytokine profiles in periodontal disease. Early studies in this context have demonstrated a higher proportion of IL-4 producing cells in periodontitis tissues suggesting a role for Th2 cells in the progressive lesion. Clonal studies have shown that the selection of a particular cytokine profile is not antigen dependent and that differences may be due to the host susceptibility although this remains to be determined. CONCLUSION: These emerging data clearly establish a role for cell-mediated mechanisms in the control of periodontal destruction and raise the possibility that in the future cytokine therapy for the treatment of periodontal disease in susceptible subjects may become a viable option.

Animals↗
PubMed1979

Definition of cellular immune responses to brain antigens in human head trauma.

Cellular immune responses to brain antigens in patients with head injury were studied by applying the leukocyte adherence inhibition (LAI) assay. The investigation was conducted in three phases. 1) In the initial phase, evaluation of a series of 22 test and 25 control cases obtained at random during a 2- to 6-week time frame following a traumatic event indicated significant non-adherence of leukocytes (NAL) in 77% of the test group and 20% of the control group in the presence of brain antigen. 2) In a second phase, larger test population was divided into four groups of different posttraumatic intervals. This study measured NAL in the presence of normal heart of normal brain antigen. Assays revealed an initial significant NAL in the presence of both antigens; however, after the first week following injury the majority of cases manifested significant NAL only with brain antigen. These values of NAL persisted over a 6- to 8-week period. 3) As a final phase of investigation, analysis of a sequential series of assays in 12 patients over a 90-day period indicated significant NAL in the presence of brain antigen within the first week of injury, this was followed by a drop in NAL in most of the cases. Studies at 7 to 60 days posttrauma demonstrated significant NAL with brain antigen alone, with a subsequent drop by 90 days. These observations are interpreted to represent sensitization of leukocyte subgroups to brain proteins that are immunologically recognized following the traumatic event.

Antibody Formation↗
PubMed1978

Lymphocyte transformation and interferon production as measures of cellular immunity in lymphoma patients.

Our studies of in vitro cellular immune responses to herpesviruses have shown that, before treatment, lymphoma patients have decreased transformation to varicella-zoster virus antigen compared to herpes simplex virus and cytomegalovirus antigens. Interferon production to varicella-zoster virus and cytomegalovirus antigens is also decreased. During the first six months of treatment, decreased lymphocyte transformation and interferon production to all herpesviral antigens was observed. Among patients in long-term remission, recovery from the suppression associated with treatment was noted except that interferon production to varicella-zoster virus antigen remained decreased.

Antigens, Viral↗
PubMedDate not supplied

An experimental study on cellular immunity and protein-calorie malnutrition.

The effect on cellular immunity of the administration of the non-specific immunopotentiator BCG and/or a streptococcal agent was studied in 90 non-cancer bearing Wistar rats under different nutritional support. The number of immunocompetent cells and the non-specific function of the immunocompetent cells significantly decreased in acute malnutrition. The non-specific immunopotentiator BCG and streptococcal agent activated the peritoneal macrophages, to a remarkable extent, but depressed spleen cell blastoid transformation, thymus index and peripheral lymphocyte count in the starved rat group. In rats who received BCG under intravenous hyperalimentation (IVH), the absolute macrophage counts went down as the quantity of amino-acid administered decreased. The acquired immunodeficiency due to acute malnutrition is evident and the effect obtained with an immunopotentiator is considered to be related to the nutritional status of the host. The adequate administration of protein-calorie is required for the effective use of the immunopotentiator.

Amino Acids↗
PubMed1994

Locus coeruleus stimulation by corticotropin-releasing hormone suppresses in vitro cellular immune responses.

Previous studies have demonstrated that stressors alter cellular immune system function, and increase the activity of locus coeruleus neurons. Furthermore, stressors increase the release of corticotropin-releasing hormone (CRH) and locus coeruleus neurons are activated by CRH. Thus, the present study examined whether activation of the locus coeruleus by infusion of CRH modulates the function of blood and spleen lymphocytes assessed in vitro. CRH (100 ng) was administered into the region of the locus coeruleus in awake rats 1 hr before spleen and peripheral blood lymphocytes were collected for culture with nonspecific mitogens. Unilateral or bilateral microinfusion of CRH into the locus coeruleus produced a decrease in blood and spleen T-lymphocyte mitogenic responses to phytohemagglutinin, ConA, and an antibody to the T-lymphocyte antigen receptor. In contrast, infusion of saline into the locus coeruleus or CRH into the surrounding region of the dorsal pons did not alter spleen or blood lymphocyte responses. Plasma concentrations of adrenocorticotropic hormone, corticosterone, and IL-6 were increased by CRH infusion into the locus coeruleus. These results suggest that CRH-evoked activation of the locus coeruleus stimulates the hypophysial adrenal axis, possibly activates the sympathetic nervous system, and results in immunosuppression. Comparable changes in lymphocyte and hormone responses are produced by an aversive stimulus or a conditioned stressor, suggesting that activation of the locus coeruleus may be a component of stressor-induced immune alterations.

Adrenocorticotropic Hormone↗
PubMed2004

Cytokines in Drosophila hematopoiesis and cellular immunity.

Hematopoiesis is a complex, multistep process in which progenitor cells undergo distinct cellular changes of proliferation and differentiation to give rise to mature blood cells in circulation. Many of the genetic and molecular events that drive these changes have been characterized in mammals, frogs, and zebra fish, and more recently in the insect model system Drosophila melanogaster. Blood cells in Drosophila are actively involved in fighting infections and the cellular immune responses are intimately tied to the process of hematopoiesis. In this article, we briefly review the fundamental similarities in Drosophila and mammalian hematopoiesis and highlight the potential roles of four cytokines/growth factors in Drosophila hematopoiesis and cellular immunity.

Animals↗
PubMed1998

Specific cellular immunity in immunocompetent children with herpes zoster.

We investigated whether specific immunity is low in immunocompetent children with zoster. Specific cellular immunity was found to be significantly lower in 13 otherwise normal children with zoster than it was in 8 matched controls by a lymphoproliferative assay. However, there was no significant difference between them with regard to the antibody response. Therefore, even in the immunocompetent children, decreased specific cellular immunity may play an important role in the mechanism of virus reactivation.

Antibodies, Viral↗
PubMed2006

Rel/NF-kappaB double mutants reveal that cellular immunity is central to Drosophila host defense.

Studies on Drosophila immunity have focused on the humoral response, whereas less is known about the Drosophila cellular immunity. Here we show that mutants that lack the Drosophila Rel/NF-kappaB proteins Dorsal and Dif have very few blood cells, are constitutively infected by opportunistic microbes, and die from infection as larvae. When the double mutants are grown in microbe-free conditions, the animals are rescued from chronic infection and many survive to adult stages. Thus, Dif and Dorsal are required for survival because they protect the animal from infection by microbes from the environment. Specific expression of Dif or dorsal in the blood cell lineage is sufficient to restore blood cell number, clear microbes, and allow survival to the adult stage. These findings demonstrate that the cellular immune response is essential for the ability of Drosophila to survive in their standard laboratory environment, and that Dif and Dorsal control crucial aspects of the cellular immune response, including blood cell survival and the ability to fight off microbial infection.

Animals↗
PubMed1975

Local adoptive transfer of the antitumor cellular immune response in syngeneic and allogeneic mice studied with a rapid radioisotopic footpad assay.

The immunologic nature of the cellular immune response against tumor cells inoculated in the footpad of mice was studied with a rapid, quantitative, and specific assay. The results indicate: a) The antitumor cellular immune response could be transferred adoptively in syngeneic and allogeneic mice with specific immune thymus (T) lymphocytes isolated on nylon columns; b) T-independent cells of host origin were necessary for the manifestation of the antitumor footpad reaction; and c) there was a close correlation between immune responses detected by the footpad assay and those detected by transplantation techniques. The footpad reaction consisted of several nonspecific and specific components. Nonspecific factors disturbing the specific footpad reaction in syngeneic and allogeneic recipients were discussed.

Animals↗
PubMed2004

Adrenergic modulation of survival and cellular immune functions during polymicrobial sepsis.

OBJECTIVE: An immunomodulatory effect of epinephrine has been reported that is supposed to be mediated via beta-adrenergic receptors. The effect of epinephrine and/or beta-adrenergic blockade on cellular immune functions during systemic inflammation has not yet been investigated. METHODS: Male NMRI mice were treated with either an infusion of epinephrine (0.05 mg/kg/h i.p.), administration of the nonselective beta-adrenoceptor antagonist propranolol (0.5 mg/kg s.c.), or a combination of epinephrine and propranolol after induction of a polymicrobial sepsis by cecal ligation and puncture. Forty-eight hours thereafter survival and cellular immune functions (splenocyte proliferation, splenocyte apoptosis and cytokine release, distribution of leukocyte subsets) were determined. RESULTS: Infusion of epinephrine did not affect lethality of septic mice but induced alterations of splenocyte apoptosis, splenocyte proliferation and IL-2 release and was associated with profound changes of circulating immune cell subpopulations. Treatment with propranolol augmented the epinephrine-induced increase of splenocyte apoptosis, did not affect the decrease of splenocyte proliferation and IL-2 release, augmented the release of IL-6 and antagonized the mobilization of natural killer cells observed in epinephrine-treated animals. Furthermore, these immunologic alterations were accompanied by a significant increase of sepsis-induced mortality. Coadministration of propranolol and epinephrine augmented the propranolol-induced changes of splenocyte apoptosis and IL-6 release and was associated with the highest mortality of septic mice. CONCLUSION: Epinephrine infusion modulated cellular immune functions during systemic inflammation without an impact on survival. A pharmacologic beta-adrenergic blockade partly augmented the epinephrine-induced immune alterations and was associated with a pronounced increase of mortality. This effect was further augmented by a combination of epinephrine infusion and beta-adrenergic blockade. These data indicate that adrenergic mechanisms modulate cellular immune functions and survival during sepsis, with these effects being mediated via alpha- and beta-adrenergic pathways.

Adrenergic beta-Antagonists↗
PubMed2003

A unique role for IL-23 in promoting cellular immunity.

Recent discoveries of interleukin (IL)-23, its receptor, and its signal-transduction pathway add to our understanding of cellular immunity. IL-23 is a heterodimer, comprising IL-12 p40 and the recently cloned IL-23-specific p19 subunit. IL-23 uses many of the same signal-transduction components as IL-12, including IL-12Rbeta1, Janus kinase 2, Tyk2, signal transducer and activator of transcription (Stat)1, Stat3, Stat4, and Stat5. This may explain the similar actions of IL-12 and IL-23 in promoting cellular immunity by inducing interferon-gamma production and proliferative responses in target cells. Additionally, both cytokines promote the T helper cell type 1 costimulatory function of antigen-presenting cells. IL-23 does differ from IL-12 in the T cell subsets that it targets. Whereas IL-12 acts on naïve CD4+ T cells, IL-23 preferentially acts on memory CD4+ T cells. This review summarizes recent advances regarding IL-23, providing a functional and mechanistic basis for the unique niche that IL-23 occupies in cellular immunity.

Animals↗
PubMed1979

Cellular immune response to acetylcholine receptor in myasthenia gravis: II. Thymectomy and corticosteroids.

We studied 11 patients with myasthenia gravis who demonstrated a cellular immune response to acetylcholine receptor (AChR) of the electric organ of Torpedo marmorata. After thymectomy, there was a marked decrease in the patients' lymphocyte reactivity to AChR. The mean reduction of the stimulation index (SI) was 50%, but the response to the nonspecific mitogen phytohemagglutinin (PHA) was not affected. In six cases, the lymphocyte response was measured at intervals up to 22 months after thymectomy; in all six, the immune response to AChR remained decreased. In some cases, the response continued to decrease, even to normal values. The effect of corticosteroid treatment was tested in other patients. The cellular immune response to AChR was significantly lower in treated patients (mean SI, 1.64 +/- 0.25) than in untreated controls (mean SI, 2.41 +/- 0.38), with no significant difference in the response to PHA. These data suggest that a decrease in the cellular immune response to AChR may be one mechanism by which thymectomy and corticosteroids are therapeutic in myasthenia.

Acetylcholine↗
PubMed1978

[The effect of cytostatic therapy with bleomycin and methotrexate on cellular immune reactivity].

Considerable importance for the elimination of malignant cells has been attributed to the cellular immune system. Cytostatic drugs however are known to be immunosuppressive. The transformation response of peripheral lymphocytes to bleomycin and methotrexate was determined before and after treatment in patients with squamous cell carcinoma of the head and neck region. The transformation response was interpreted as an indication of the potential for the nonspecific cellular immune reaction. The cellular reaction was significantly suppressed during therapy; this suppression was then followed by an excessive reaction in some patients. The immunosuppressive effect of bleomycin was substantiated in in vitro studies of isolated lymphocytes from healthy doners. Low concentrations of methotrexate however produce excessive reactions while higher concentrations tend to have an immunosuppressive effect.

Bleomycin↗
PubMed1978

Abnormalities in humoral and cellular immunoactivity in pancreatitis. II. Study of the cellular immune system.

The in vitro parameters of the cellular immune system were followed up during the course of, and over 1 to 8 months after recovery from acute pancreatitis and in chronic pancreatitis. In acute pancreatitis, a significant inhibition of leucocyte migration and a significant reduction of the percentage and absolute number of early and total rosette-forming (T) lymphocytes were demonstrated. These abnormalities ran parallel with the alterations of the humoral immune system described in the first paper of this series. On the evidence of the follow-up studies continued for 1 to 8 months, the abnormalities of the cellular and humoral immune system were found to persist in the majority of the cases. The same is valid for chronic pancreatitis. The possible causes of the abnormalities are discussed. Tentative interpretations are offered for the possible role of specific immune sensitization in the transition of the acute to the chronic inflammatory process and in the progression of chronic inflammation.

Cell Migration Inhibition↗