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PubMed1992

Enhancement of cellular immune function during cold adaptation of BALB/c inbred mice.

The cell-mediated immune function of cold-adapted BALB/c inbred mice was studied in experiments of splenic lymphocyte blastogenesis, indicated by tritium-labeled deoxythymidine incorporation and SDS-PAGE autoradiography of synthetic proteins in lymphocytes. Male BALB/c inbred mice were randomly divided into two groups: control (living at 25 degrees C) and cold-exposed (living at 2 degrees C). Results are as follows: in contrast with the control group, there was an obvious fluctuation of cell-mediated immune function in the cold-exposed group at initial cold exposure because of transient stress to cold; then cell-mediated immune function gradually recovered to control level. From Day 15, the cell-mediated immune function of the cold-exposed group was remarkably enhanced. On Day 15, the lymphocyte blastogenesis rate was increased by 20.66% (P less than 0.05), which implies the onset of cold adaptation; on Days 21 and 31, the rates increased by 80.15% (P less than 0.05) and 40.36% (P less than 0.05), respectively. Two to six months later, with continuing cold exposure, the murine lymphocyte blastogenesis rate in the cold-exposed group remained higher than that in the control group. The lymphocyte protein synthesis of the cold-exposed group, indicated by tritium-labeled leucine incorporation, apparently increased on Day 15 and the stimulated rate was 101.47% (P less than 0.05). SDS-PAGE autoradiography of synthetic proteins in lymphocytes demonstrated that after 2 weeks of cold exposure, protein bands were enriched in both quantity and quality. These results are identical to the results obtained from lymphocyte blastogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗

PubMed1988

Lack of a relationship between immune function and chemically induced hepatocarcinogenesis in B6C3F1 mice.

The relationship between immune function and chemically induced hepatocarcinogenesis was studied employing an in vivo murine model. Neonatal B6C3F1 mice were given a single carcinogenic dose of diethylnitrosamine (DEN) and the time-response kinetics for the early (foci of alteration) and late (adenomas/carcinomas) phases of hepatocellular carcinogenesis were compared to changes in hematopoiesis and immune functions associated with immune surveillance and natural resistance. Increases in hematopoiesis occurred just prior to or concurrent with the appearance of hepatocellular carcinomas, while increased macrophage and natural killer cell cytotoxicity and suppression of cell-mediated immunity occurred following tumor appearance and progressed with increasing tumor burden. Neither immunological nor hematopoietic changes were associated with early phases of hepatocarcinogenesis, as monitored by the appearance of altered hepatocellular foci. Although changes in hematopoiesis may represent an early indicator for hepatocarcinogenesis in the mouse tumor model, the data suggest that altered immune surveillance and natural resistance are not factors in the development of chemically induced hepatocellular tumors, and the changes in immune function are probably secondary to tumor development.

Animals↗

PubMed1992

[Determination of red blood cell immune functions in patients with pulmonary tuberculosis].

Red blood cell immune functions were determined in 106 patients with pulmonary tuberculosis (tbc) and in 37 blood donors as a control group. In control group, RBC-C3bRR was 17.2 +/- 6.5%, RBC-ICR was 4.0 +/- 2.2%. In the group, both RBC-C3bRR and RBC-ICR levels were elevated in 23 patients, only RBC-C3bRR level or RBC-ICR level rose in 40 or 31 cases respectively. so, 88.6% of patients showed elevation of RBC immune function. The pathological changes were also correlated with the level of RBC-ICR, RBC-C3bRR significantly (P < 0.01). The authors suggested that the measurement of RBC immune functions might be useful in diagnosis, assessment of the severity and outcome of pulmonary tuberculosis.

Adolescent↗

PubMed1991

[Effect of growth hormone on immune function in normal and hypophysectomised rats].

The effect of growth hormone (GH) on immune function was studied using normal and hypophysectomised male Wistar rats. Hypophysectomy was performed by the auditory approach at 4 weeks of age. Normal and hypophysectomised rats were treated with saline or 0.4IU/body GH daily during 7 to 11 weeks of age. Histological features of the thymus and spleen and immunological parameters including blood cell counts, lymphocyte subsets, serum immunoglobulin levels, splenic natural killer activity, and mitogen-induced splenic lymphocyte proliferation were examined in the rats at 11 weeks of age. In hypophysectomised rats, the counts of peripheral white blood cells (5,513 +/- 813/microliters), lymphocytes (4,838 +/- 737/microliters), Th/i cells (2,237 +/- 329/microliters), and B cells (1,400 +/- 509/microliters), Th/i/Ts/c ratio (1.78 +/- 0.27), splenic T cell subsets (pan T: 51.0 +/- 4.3%, Th/i: 31.6 +/- 3.0%, Ts/c: 23.9 +/- 2.7%), and serum IgG level (2,148 +/- 470mg/l) were significantly decreased as compared with normal rats. Natural killer activity (17.8 +/- 4.6%) and mitogen-induced proliferation of T cells (Con A: 47.1 +/- 15.7, PHA: 51.6 +/- 12.5) were also suppressed. Hypoplasia of the thymus and spleen was observed in parallel to retarded growth of the rats. In contrast, GH supplement to the hypophysectomised rats resulted in increases in growth and lymphoid tissue, and the restoration of the counts of peripheral white blood cells (6,850 +/- 840/microliters), lymphocytes (6,211 +/- 731/microliters), Th/i cells (2,909 +/- 304/microliters), and B cells (1,947 +/- 402/microliters), Th/i/Ts/c ratio (2.04 +/- 0.34), serum IgG level (3,414 +/- 1,326mg/l), and natural killer activity (25.7 +/- 4.7%). However, splenic lymphocyte subsets and mitogen-induced proliferation of T cells were not recovered by GH treatment for 4 weeks. GH administered to normal rats increased serum IgG level (4,982 +/- 1,496mg/l) but did not affect other immunological parameters. These results indicate that humoral and cell-mediated immune function are impaired in hypophysectomised rats, but GH supplement administered to them restored most of the impaired immune function, suggesting that GH plays an important role in the development of immune function.

Animals↗

PubMed1990

The first Icelandic family with X-linked agammaglobulinaemia: studies of genetic markers and immune function.

This paper describes studies of genetic markers and immune functions in the first Icelandic family identified with X-linked agammaglobulinaemia (X-LA), including three affected brothers. The eldest brother was diagnosed at the age of 9 in 1963. He suffered repeated infections and died at the age of 23. The other two affected brothers, diagnosed at 6 years and 1 year of age, are alive and well on immunoglobulin replacement therapy at the ages of 32 and 24. All were typed for HLA, complement, and various other markers. Pedigree analysis suggests an X-linked segregation of the disease. Their serum IgG is maintained at normal levels on therapy. Several parameters of immune function were studied. The following results were obtained for the X-LA brothers: B cells are absent in their peripheral blood samples. T-cell numbers are normal, but monocytes are increased in numbers and activity. No immunoglobulin production could be elicited in vitro with PWM and no cells containing cytoplasmic Ig were detectable among PWM-stimulated blasts. Nevertheless the proliferative response was particularly vigorous, but the responding cells were shown to be exclusively T cells. No blast transformation could be achieved with EB virus. NK-cell activity was normal/high normal. Other cell-mediated immune functions were normal. In conclusion our data indicate that the differentiation of B cells is blocked in the two surviving X-LA brothers. They have survived for a longer time and in better health than is generally reported. Early diagnosis and adequate replacement treatment with Ig is clearly crucial. Vigorous non-specific immune mechanisms may help to compensate for the defective specific immunity.

Agammaglobulinemia↗

PubMed1990

Aging effect on the immune functions of murine gut-associated lymphoid tissues.

Immune functions generally decline with aging. However, the onset and the rate of the functional decline may be different in each lymphoid compartment. We studied the effect of aging on the murine Peyer's patch (PP) cells, and mesenteric lymph node (MLN) cells, which are a part of gut-associated lymphoid tissues (GALT). The capacity of proliferative responses to mitogens of lymphoid cells from GALT decreased with aging. However, the rate of the decrease was much slower than that in the spleen cells. Production of interleukin-2 (IL-2) and interleukin-3 (IL-3) in aged T cells was also studied. IL-2 production of T cells from PP, MLN, spleen cells decreased with age. The age-related decrease was observed at 21 months of age in spleen and at 24 months of age in PP and MLN cells. In contrast, IL-3 production of PP, MLN, spleen cells didn't decrease at 21 months of age, but decreased only in spleen cells at 24 months of age. Therefore, it is suggested that the onset and the rate of age-related functional decline of GALT are much later and slower than those of systemic immune system. GALT seems to maintain the immune functions longer than systemic immune system.

Aging↗

PubMed1992

Transfer of the ADA gene into human ADA-deficient T lymphocytes reconstitutes specific immune functions.

Peripheral blood lymphocytes obtained from a patient affected by adenosine deaminase (ADA) deficiency and severe combined immunodeficiency were infected with a retroviral vector containing two copies of a human ADA minigene, and injected into bg/nu/xid (BNX) immunodeficient mice. Six to 10 weeks after injection, human T cells were cloned from the spleens of recipient animals and analyzed for proliferative potential, T-cell surface markers, expression of ADA activity, integration of retroviral sequences, T-cell receptor (TCR) beta gene rearrangement, and specificity of antigen recognition. Efficient gene transfer and expression restored proliferative potential in vitro and long-term survival in vivo. All clonable human T lymphocytes obtained from the spleen of recipient animals had high levels of vector-derived ADA enzyme activity and showed predominantly the CD4+ phenotype. Retroviral integrations and TCR-beta gene rearrangements demonstrated the presence of a variety of different clones in the spleens of recipient mice. Furthermore, the combined analyses of vector integration and TCR rearrangement provided evidence that a circulating progenitor cell was transduced by the retroviral vector, giving rise to different and functional TCRs. Evaluation of antigen-specificity demonstrated both alloreactive and foreign antigen specific immune responses. These results suggest that restoration of enzyme activity in human ADA-deficient peripheral blood T cells by retroviral-mediated ADA gene transfer allows in vivo survival and reconstitution of specific immune functions. Therefore, retroviral vector-mediated gene transfer into circulating mononuclear cells could be successful not only in maintaining the metabolic homeostasis, but also for the development of a functional immune repertoire. This is a fundamental prerequisite for the usage of genetically engineered peripheral blood lymphocytes for somatic cell gene therapy of ADA deficiency.

Adenosine Deaminase↗

PubMedDate not supplied

Immune function and nutrition. The clinical role of the intravenous nurse.

Protein-calorie malnutrition is considered to be one of the most frequent causes of immunosuppression in the world today. Malnutrition can affect the functioning of T cells, B cells, and macrophages, the principle players involved in cell-mediated and humoral immunity. Immune function is measured by the total lymphocyte count and delayed cutaneous hypersensitivity reaction. Nutritional markers include serum albumin and transferrin levels. Immune function is affected by protein (especially arginine intake); the balance between omega-6 and omega-3 fatty acid intake; and adequate amounts of vitamins A, E, and C, and the minerals zinc and iron. A deficiency of these nutrients puts the patient at increased risk of infection. Non-nutritional factors can influence immune functioning as well. The intravenous nurse must review the patients history, physical examination, and laboratory values to achieve a global view of the patient's immune function and nutrition status in order to be able to develop an appropriate care plan based on this nursing diagnosis: potential for infection secondary to alteration in immune function.

Antibody Formation↗

PubMed1987

Immune function in spinal cord-injured males.

Infected and noninfected spinal cord-injured (SCI) patients, bilateral amputees (control for mobility), and a control group were compared for immune function. Immune measures involved acute phase reactants (erythrocyte sedimentation rate [ESR], c-reactive protein [CRP], and alpha-1 globulin [A1G], T cell measurements (absolute lymphocyte count [ALC]), and B cell function (gamma globulin [GG]). All subjects were at least three months postinjury, had no history of immune system disease, and were not taking potential immune system altering drugs. There was no T or B cell dysfunction, but acute phase reactants were elevated, even in patients without infection. Criteria for predicting infection included recent injury, few previous infections, and catheters. The best predictor of infection was CRP. Suggestions for further research include investigating nonhospitalized patients, searching for reasons for elevated acute phase reactants, and using the predicting formula on newly injured patients to see if it predicts infectious complications.

Adult↗

PubMed1989

Effect of copper on immune function and disease resistance.

Recent evidence suggests that copper exacts an important role in the maintenance of immunocompetence. Copper deficiency results in decreased humoral and cell-mediated, as well as nonspecific immune function. Impairment of immune function may be highly correlated with an increased incidence of infection and higher mortality rates observed in copper-deficient animals. The actual mechanisms by which copper is involved in immune processes are not well defined. This review addresses the copper-immune function interaction and discusses possible immunomodulatory roles for copper.

Animals↗

PubMed1991

[Changes in T-lymphocyte subsets in patients with orthopedic trauma and effects of yipanzhu decoction on the impaired immune function].

The effects of yipanzhu decoction (YD) on immune function in 40 patients [2 groups, YD and normal saline (NS) group] with orthopedic trauma by taking T lymphocyte subsets as indexes were observed. The peripheral venous blood samples randomly taken from 30 healthy subjects served as control. The blood were collected within 24 hours after trauma. Then the YD and NS were respectively given to the patients in the 2 groups for 3 days, and the blood were taken 4th, 7th, 14th day after trauma for the observation of T subsets. The results revealed that before administration of YD the percentage of pan-T cells was reduced with an increased percentage of Ts cells and a decreased ratio between Th and Ts cells; 3 days after giving the drugs in YD group the percentage of pan-T cells was slightly increased, and the changed percentage of Ts cells and the ratio of Th/Ts cells mentioned above was recovered to normal, while in NS group all these indexes remained at abnormal range during the period we observed. The results suggested that YD could promote the recovery of abnormal T lymphocyte subsets in traumatized patients, and it possessed to some extent the function of immune regulation that was helpful to reduce the ratio of infection after trauma.

Adolescent↗

PubMed1989

Effect of age on epidermal immune function.

Like other systems in the body, the immune system deteriorates with age. Age-related changes in epidermal immune function include morphologic and functional changes in Langerhans cells, decreased production and response to epidermal thymocyte-activating factor (ETAF), and altered allergic contact dermatitis. These may be primary age-related changes in epidermal immune function or may be secondary to aging of the organism. In either case, the age-related changes in epidermal immunity may contribute to the increased susceptibility to cutaneous infections and neoplasms with advancing age.

Aging↗

PubMed1986

Effect of age on epidermal immune function.

Aged↗

PubMed1992

Modulation of age-related alterations in membrane composition and receptor-associated immune functions by food restriction in Fischer 344 rats.

Food restriction is known to modulate aging and age-associated immune functions in rodents. In an attempt to understand the mechanism(s) through which food restriction delays age-associated loss of certain immune functions, lipid composition of spleen cells as well as binding of spleen cells to interleukin-2 (IL-2) and insulin were analyzed in four month-old and 19-month-old ad libitum fed (AL) and food-restricted (FR) Fischer-344 male rats. The results revealed that although AL-fed rats did not show a difference in age-related changes for IL-2 and insulin binding, the number of binding sites were significantly increased in the spleen cells of 19-month-old FR animals when compared with those of the 19-month-old AL group. When spleen cell phospholipid fractions were analyzed for fatty acid composition, the spleen cells from FR animals consistently revealed higher linoleic acid (18:2) levels and significantly lower arachidonic acid (20:4) and long chain fatty acid, docosatetraenoic acid (22:4) levels in the phosphatidylcholine and phosphatidylethanolamine fractions than the spleen cells of the AL rats. Further, spleen cell plasma membranes of FR rats also exhibited similar changes showing higher 18:2 and lower 20:4 and 22:4 levels than the AL animals. Finally, spleen cells obtained from 19-month-old FR animals produced higher levels of IL-2 and lesser prostaglandin E2 when compared to 19-month-old AL animals. The above observations suggest that one of the mechanisms through which food restriction may delay the loss of age-associated immune functions is through modulation of the fatty acyl composition of phospholipid fractions of spleen cell membranes. This modification may facilitate binding of IL-2 and insulin to their receptors and thus may improve T cell proliferation and prevent or delay age-related loss in immune functions.

Aging↗

PubMed1983

Cellular immune function in rheumatic disease.

Investigation of the cellular immune function in patients with rheumatic diseases is important in elucidating the pathogenesis of the disease processes and in determining the associated abnormalities of recognition and regulation exerted by the immune system. However, because of the lack of specificity and the variations noted from laboratory to laboratory, tests of cellular immune function are, at present, of little value in the laboratory diagnosis of these diseases. The abnormalities found in the rheumatic diseases occur with many autoimmune diseases and other inflammatory states. The common pathway of immune abnormalities appears to be influenced by several factors. They include several genetic loci, possible environmental factors, and immunologic mechanisms, which appear to interact in an intimate way to induce various autoimmune diseases.

Arthritis, Rheumatoid↗

PubMed1991

Association of vitamin B6 status with parameters of immune function in early HIV-1 infection.

Nutritional deficiencies have been documented to affect immune function. The present study indicates that vitamin B6 deficiency is prevalent in CDC stage III HIV-1-infected subjects, despite adequate dietary vitamin B6 intake. As vitamin B6 deficiency has been previously shown to affect immune function, these relatively asymptomatic HIV-1-infected patients were examined for evidence of a relationship between vitamin B6 deficiency and immune dysregulation. Vitamin B6 status in HIV-1-infected subjects was significantly associated with functional parameters of immunity [multivariate F(3,36) = 3.70, p less than or equal to 0.02]. Additional analyses indicated that overtly deficient participants exhibited significantly decreased lymphocyte responsiveness to the mitogens phytohemagglutinin and pokeweed, and reduced natural killer cell cytotoxicity, compared to subjects with clearly adequate vitamin B6 status (chi 2 = 8.78, df = 3, p less than 0.04). Vitamin B6 status was not related to immune cell subpopulations, e.g., CD4, CD8 cell number, or level of serum immunoglobulins. The results of this study indicate that while vitamin B6 status is not a primary etiological factor in HIV-1-related immunological dysregulation, it appears to be an important cofactor of immune function.

Acquired Immunodeficiency Syndrome↗

PubMed1991

Immune function in growth hormone-deficient children treated with biosynthetic growth hormone.

Conflicting data regarding the immune function in growth hormone (GH) -deficient children or changes in immune parameters during substitutive GH therapy have been reported. We have studied the immune function in 13 patients with GH deficiency before and during treatment with biosynthetic GH (12 IU/m2 body surface/week) after 6 and 12 months of therapy. We found that the absolute number of total T lymphocytes and T-cell subsets (using monoclonal Ab as markers), Natural Killer cell activity (target K562) and response of lymphocytes to polyclonal mitogens (PHA, ConA, PWM) were all in the normal range and remained so after 6 and 12 months of therapy. The absolute number of B lymphocytes was in the normal range before treatment and after 6 months of therapy but dropped significantly after 12 months of treatment. Serum immunoglobulins (IgG, IgA, IgM) did not show a parallel drop and remained normal throughout the whole study. Our GH-deficient patients did not show any undue susceptibility to infections and our data thus seem to confirm that the immune function is basically intact in these children and that it is not suppressed by GH treatment. Although a drop in B lymphocytes was observed, the normal level of immunoglobulins and the normal functional response to PWM seem to demonstrate the maintenance of a normal humoral immune response.

Adolescent↗

PubMed1985

Epidermodysplasia verruciformis associated with Bowen's carcinoma, B lymphocytopenia and decreased immune functions.

A case of epidermodysplasia verruciformis associated with Bowen's carcinoma, persistent B lymphocytopenia and decreased immune functions is reported. Human papilloma virus 5 (HPV-5) DNA was shown to be associated with the DNA from the tumor tissue by Southern blot hybridization using P-labeled HPV DNA sequences cloned on plasmid vectors. The associated Bowen's carcinoma in our case may be caused by multiple-factor relationships which include (a) an oncogenic potential of infected virus; (b) an inherited abnormality in immune function, and (c) the decreased immune function resulting from the viral infection itself. A marked B lymphocytopenia appears to be associated with persistent viral infection.

Aged↗