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At least 1,621 records · Page 90Linked to original sources
PubMed1991

Augmentation of cellular immune function during the early phase of zidovudine treatment of AIDS patients.

Twenty-five patients with AIDS in AIDS Clinical Trials Group Protocol 002 were treated with either low or high dosages of zidovudine. This resulted in moderate, transient increases by 10 and 20 weeks in lymphocyte blastogenesis and interferon-gamma (IFN-gamma) production in vitro in response to phytohemagglutinin with and without recombinant interleukin-2. Immune responses to cytomegalovirus and herpes simplex virus type 1 antigens were augmented less frequently during therapy. Natural killer (NK) cell lysis of uninfected and human immunodeficiency virus-infected cells was also transiently increased by 10 and 20 weeks. IFN-gamma production, the only immune parameter directly associated with increases in numbers of CD4+ T cells, peaked at 10 weeks of treatment. The limited efficacy of zidovudine treatment in AIDS patients is associated with moderate, temporary increases in nonspecific and herpesvirus-specific T lymphocyte responses and NK cell function.

Acquired Immunodeficiency Syndrome↗
PubMed2005

Budesonide, but not tacrolimus, affects the immune functions of normal human keratinocytes.

Topical immunosuppressant therapy is widely used in the treatment of inflammatory skin diseases such as psoriasis and atopic dermatitis. Besides its beneficial therapeutic effects, application of topical anti-inflammatory drugs may render the epidermis more vulnerable to invading pathogens by suppressing innate immune responses in keratinocytes, such as cytokine production and Toll-like receptor (TLR) expression. In order to evaluate and compare the immunosuppressive effects of different immunosuppressant drugs on keratinocytes, we treated lipopolysaccharide (LPS)-stimulated and -unstimulated normal human keratinocytes with the synthetic corticosteroid budesonide and the macrolide tacrolimus. The expressions of the pattern recognition receptors (PRRs) TLR2 and TLR4 were measured by quantitative RT-PCR, pro-inflammatory cytokines IL-1alpha, IL-8 and TNF-alpha were monitored by quantitative RT-PCR and by ELISA, and alterations in TLR2 protein level were measured by flow cytometry. Budesonide had a suppressive effect on both constitutive and LPS-induced IL-8 gene expression. The amount of TNF-alpha mRNA was diminished in unstimulated keratinocytes, while TLR2 mRNA expression was markedly enhanced both in unstimulated and LPS-treated cells after incubation with budesonide. This increase in TLR2 mRNA expression was also detectable at the protein level in LPS-stimulated cells. Tacrolimus had no effect on any of the examined genes. Budesonide, but not tacrolimus, significantly inhibited the NF-kappaB-dependent luciferase reporter activity in HaCaT cells after induction with LPS or TNF-alpha. Although tacrolimus and budesonide are both effective treatments in some inflammatory skin diseases, the data provided here imply differences in local therapeutic and adverse effects of these two topical immunosuppressants.

Anti-Inflammatory Agents↗
PubMed1982

Yeast killer plasmid mutations affecting toxin secretion and activity and toxin immunity function.

M double-stranded RNA (MdsRNA) plasmid mutants were obtained by mutagenesis and screening of a diploid killer culture partially heat cured of the plasmid, so that a high proportion of the cells could be expected to have only on M plasmid. Mutants with neutral (nonkiller [K-], immune [R+]) or suicide (killer [K+], sensitive [R-] phenotypes were examined. All mutants became K- R- sensitives on heat curing of the MdsRNA plasmid, and showed cytoplasmic inheritance by random spore analysis. In some cases, M plasmid mutations were indicated by altered mobility of the MdsRNA by agarose gel electrophoresis or by altered size of in vitro translation products from denatured dsRNA. Neutral mutants were of two types: nonsecretors of the toxin protein or secretors of an inactive toxin. Of three neutral nonsecretors examined, one (NLP-1), probably a nonsense mutation, made a smaller protoxin precursor in vitro and in vivo, and two made full-size protoxin molecules. The in vivo protoxin of 43,000 molecular weight was unstable in the wild type and kinetically showed a precursor-product relationship to the processed, secreted 11,000-molecular-weight toxin. In one nonsecretor (N1), the protoxin appeared more stable in a pulse-chase experiment, and could be altered in a recognition site required for protein processing.

Hot Temperature↗
PubMed2002

A CD45 minigene restores regulated isoform expression and immune function in CD45-deficient mice: therapeutic implications for human CD45-null severe combined immunodeficiency.

Transgenic mice have been generated that carry a CD45 minigene under control of the human leukocyte function-associated antigen (LFA-1, CD11a) promoter. CD45-null mice carrying the transgene exhibit the lymphocyte lineage-specific isoform expression patterns of wild-type mice. Furthermore, these mice have normal thymocyte development and peripheral T-cell numbers. The proliferative ability of T cells in response to mitogens and antigen also is regained, as is B-cell responsiveness to anti-IgM. The antibody response to antigen is also restored and is similar to that of normal mice. Therefore, introduction of a functional CD45 minigene is sufficient to overcome the principal severe combined immunodeficiency (SCID)-associated defects and represents a potential route to a gene therapy for human CD45-deficent SCID.

Animals↗
PubMed2000

Improved immune functions with administration of a low-fat diet in a burn animal model.

The purpose of this study was to characterize the impact of a low-fat (LF; 1% fat) diet, a high-fat (HF; 25% fat) diet, and a standard (SD; 5% fat) diet on immune and oxidative parameters in a 20% body surface area burn animal model fed ad libitum for 10 days postinjury. Although the mechanisms are poorly understood, the amount of dietary lipid in nutritional support has been shown to have immunomodulatory effects after burn injury. Burned mice fed the LF diet showed a normal response in activated splenocyte proliferation compared to burned animals that received the SD or HF diet. Animals fed the SD and HF diets presented increased production of nitric oxide and prostaglandin E2 response after burn injury, which is associated with inhibited splenocyte proliferation. The total thiol concentration in spleen cells from burned animals kept on the HF diet was significantly higher than that in unburned animals, while no increase in these oxidative parameters was observed in LF-fed burned animals. Moreover, the LF diet significantly reduced hepatic lipid peroxidation, as measured by malonaldehyde concentration, compared to the other two diets. These results suggest that the administration of a LF diet in mice after a burn injury prevents inhibition of in vitro splenocyte proliferation and reduces the intensity of oxidative stress.

Animal Feed↗
PubMed2000

Venom from the endoparasitic wasp Pimpla hypochondriaca adversely affects the morphology, viability, and immune function of hemocytes from larvae of the tomato moth, Lacanobia oleracea.

During oviposition, the endoparasitic wasp Pimpla hypochondriaca injects its pupal hosts with venom. This complex fluid has toxic properties and recently several venom components were characterized. In addition, it was suggested that venom might be involved in host immune suppression. For this to be the case, venom would have to adversely affect hemocytes and this aspect was further addressed in the current study utilizing the larval stage of the tomato moth Lacanobia oleracea as a model system. Using sublethal venom injections we investigated the effects of venom on encapsulation and hemocyte concentration. Additionally, the effects of venom on hemocyte morphology, viability, and phagocytic capability were determined in vitro. Injection of 16 microg of venom protein into sixth instar larvae was sufficient to reduce the ability of hemocytes to encapsulate Sephadex A25 beads by more than 50% in four of five insects examined. Hemocyte concentration in sixth instar larvae 32 h after injection with 16 microg of venom was reduced by 56% compared to that in controls. Damaged hemocytes and cell debris were also observed in hemolymph from venom-treated insects, suggesting that P. hypochondriaca venom has cytotoxic properties. In vitro incubation of washed hemocytes for 20 h with 500 ng/microl venom resulted in disintegration of a high proportion of hemocytes, leaving only parts of the plasma membrane and nucleus intact. Treatment with low concentrations of venom (1.6 ng/microl) resulted in an absence of spread plasmatocytes, which were abundant on control monolayers. High-resolution microscopy of hemocyte cultures exposed to 320 ng/microl venom for 3.5 h on glass slides indicated that venom induced a variety of effects on cellular morphology, including blebbing of the plasma membrane, degranulation, and the formation of cytoplasmic vacuoles. Incubation of hemocytes with 320, 64, or 3.2 ng/microl venom for 3.5 h reduced cell viability to 70, 90, and 92%, respectively, confirming that venom is cytotoxic to hemocytes. Treatment with 320 ng/microl venom reduced the capacity of hemocytes to phagocytose Escherichia coli by 85%. Together, these results demonstrate that at sublethal doses venom has a potent anti-hemocyte action and can impair hemocyte-mediated immune responses.

Animals↗
PubMed1983

Cell-mediated immune functions, interleukin 2 and interferon production by high leukemia incidence mutant (hr/hr) mice of the HRS/J strain.

Homozygous hr/hr mice of the HRS/J strain have a high incidence of lymphoma not seen in congenic hr/+ littermates. The suggestion has been made that a helper T cell defect in the immune system of the homozygotes may account for this. To further examine the immune status of these mice, we compared the ability of spleen cells of mice of both types to stimulate, as well as to generate, allogeneic cell-mediated cytolytic responses and to produce a soluble mediator of such responses. In addition, both types of mice were tested for their ability to produce interferon (IFN) or to have their splenic natural killer cell (NK) levels augmented by polyriboinosinic-polyribocytidylic acid (poly rI-rC). We found that the spleen cells of young or aging mice of either type were able to stimulate the generation of alloreactive cytotoxic cells, but they did not inappropriately stimulate the generation of syngeneic cytotoxic cells. Similarly, spleen cells of both types of mice produced a T helper cell-derived growth factor (interleukin 2) involved in the proliferation of cytolytic cells and generated a classical cell-mediated lympholysis (CML) response to alloantigen-bearing cells. Finally, spontaneous NK cell levels, as well as poly rI-rC augmented IFN and NK cell levels, were similar in both types of mice. Thus, it appears that if defects in the immune system are solely responsible for the high incidence of lymphoma in hr/hr mice, the defects involve components or regulatory aspects of that system that have yet to be defined.

Animals↗
PubMed1985

Local and regional immune function of vitamin A-deficient rats with ocular herpes simplex virus (HSV) infections.

Experimental ocular herpes virus (HSV) infections are more severe in vitamin A-deficient rats (-A) compared with normal pair-fed controls (+A). In an effort to determine whether alterations in specific or nonspecific immune responses were responsible for the increased susceptibility of -A rats, cell-mediated responses and natural killer cell (NK) activity were monitored during the course of ocular herpetic infections in -A and +A rats. Prior to infection the concanavalin A (Con A)-induced response of splenic lymphocytes from -A rats was significantly less than that of +A animals. Three days following topical application of HSV to abraded corneas, the Con A-induced splenic response decreased in both -A and +A animals and remained at low levels for 10 d following infection. The cervical lymph node (CLN) response to Con A was depressed 7 d following infection but was higher in the -A group than in the +A group at all time points. In vitro response to inactivated HSV antigen appeared on d 7 in the spleen and d 10 in the CLN. The responses were higher in -A animals compared with +A pair-fed controls and were related to the severity of the disease rather than to dietary treatment. Splenic NK cytotoxic responses were higher in +A than -A animals and decreased in both groups during the 10-d post-infection period. Cervical lymph node NK responses were unaffected by diet or ocular HSV infection.

Animals↗
PubMed1975

Quantitation of T and B lymphocytes and cellular immune function in Hodgkin's disease.

Peripheral blood T and B lymphocytes were quantitated in 42 patients with untreated Hodgkin's disease and the results compared with the response to phytohemagglutinin (PHA) stimulation and delayed hypersensitivity skin testing. T lymphocytes were identified by an in vitro cytotoxicity assay employing a specific anti-T-cell serum and by spontaneous rosette formation with sheep erythrocytes (E rosettes). The percentage of T cells in the patients was similar to that of normal subjects as judged by the cytotoxicity assay (65 to 90%). In addition, absolute T-lymphocyte counts were normal in 63% of the patients and were generally reduced only in those with lymphopenia. The percentage of T lymphocytes determined by the E-rosette assay was similar to that determined by the cytotoxicity assay in normal controls, but was significantly lower than that determined by the cytotoxicity assay in the patients. Moreover, the decreased response to PHA stimulation in the patients was directly correlated with the decrease in E-rosette formation. These findings suggest that T lymphocytes in the peripheral blood are not generally diminished in untreated Hodgkin's disease. However, a proportion of these cells exhibits altered surface interactions that may account for some aspects of their impaired immunologic function.

B-Lymphocytes↗
PubMed1987

Effect of misoprostol on immune function in elderly subjects.

The immunologic effects of misoprostol, an oral prostaglandin E1 (PGE1) analog, were tested in 25 individuals over age 65, compared to 25 individuals given placebo. Elderly subjects were chosen because previous in vitro studies had found an increased sensitivity to PGE of lymphocytes in older subjects. After two weeks of ingestion of misoprostol or placebo, there was a small but statistically significant decrease in IgM-rheumatoid factor in the misoprostol group when compared to control and a significant decrease in the in vitro sensitivity of lymphocytes from the misoprostol group to inhibition by PGE. There were no differences in total lymphocyte count, T cell or T cell subset count, delayed hypersensitivity skin test reactivity, serum immunoglobulins, or response to mitogens between the two groups. Therefore, the short term administration of an oral PGE analogue to normal elderly individuals is not associated with any detrimental effects on immunologic function after two weeks.

Aged↗
PubMed1994

Probing immune functions in RAG-deficient mice.

Inactivation of recombination activating gene (RAG)-1 or RAG-2 in mice results in the inability of developing lymphocytes to initiate V(D)J recombination, leading to the arrest of lymphocyte differentiation at a very early stage. Introduction of functionally assembled antigen-receptor genes or other potentially relevant genes into the RAG-deficient background can bypass the V(D)J recombination block and promote differentiation of the lymphocytes of RAG-deficient mice to various stages. This approach offers new means for analyzing the control of lymphocyte differentiation. In addition, generation of somatic chimeric mice by injecting mutant embryonic stem cells into the RAG-2-deficient blastocysts has also provided a powerful new method for assaying the potential roles of genes or regulatory elements in lymphocyte development or function.

Animals↗
PubMed2001

Iron biology in immune function, muscle metabolism and neuronal functioning.

The estimated prevalence of iron deficiency in the world suggests that there should be widespread negative consequences of this nutrient deficiency in both developed and developing countries. In considering the reality of these estimates, the Belmont Conference seeks to reconsider the accepted relationships of iron status to physiological, biochemical and neurological outcomes. This review focuses on the biological processes that we believe are the basis for alterations in the immune system, neural systems, and energy metabolism and exercise. The strength of evidence is considered in each of the domains and the large gaps in knowledge of basic biology or iron-dependent processes are identified. Iron is both an essential nutrient and a potential toxicant to cells; it requires a highly sophisticated and complex set of regulatory approaches to meet the demands of cells as well as prevent excess accumulation. It is hoped that this review of the more basic aspects of the biology of iron will set the stage for subsequent in-depth reviews of the relationship of iron to morbidity, mortality and functioning of iron-deficient individuals and populations.

Anemia, Iron-Deficiency↗