Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Immune function”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,783 records · Page 99Linked to original sources
PubMed2001

Immune function in Swedish élite orienteers.

During 1979-1992 an increased frequency of sudden unexpected cardiac death (SUD) occurred among young male Swedish élite orienteers. Subacute-to-chronic myocarditis was found in 12/16 (75%) at autopsy and Chlamydia pneumoniae, or a cross-reacting agent, was suspected on the basis of diagnostic tests performed. Because myocarditis is an infrequent cause of SUD and clusters of SUD are rare, whereas Chlamydia pneumoniae infections are ubiquitous and seldom cause severe myocarditis, 119 top ranked élite orienteers (67 males and 52 females) and 36 highly trained male middle-distance runners and cross-country skiers, serving as controls, underwent immunologic screening in an effort to reveal possible immune dysfunction. Except for two orienteers and one runner/skier who showed genetic C3-deficiency or IgA-deficiency, the results showed no significant differences between the orienteers and controls with respect to immunoglobulin levels, complement activation, lymphocyte subsets, including activated T lymphocytes, and sIL-2r-alpha. IL-1 beta, IL-6, TNF-alpha, and sCD8, tested in the orienteers only, were normal. However, IFN-gamma was significantly higher in controls than in orienteers, who showed normal levels, whereas the orienteers had increased sELAM-1 and sICAM-1 levels. Finally, sIL-2 receptor-alpha was similarly elevated in orienteers and controls. We conclude that, with the tests employed, no immunologic disturbance could be revealed in the orienteers that may potentially have increased their susceptibility to myocarditis and SUD.

Adolescent↗
PubMed2002

Supplemental fructooligosaccharides and mannanoligosaccharides influence immune function, ileal and total tract nutrient digestibilities, microbial populations and concentrations of protein catabolites in the large bowel of dogs.

The goal of this study was to examine whether supplemental fructooligosaccharides (FOS) and (or) mannanoligosaccharides (MOS) influenced indices of gut health of dogs. Adult female dogs (n = 4) surgically fitted with ileal cannulas were fed a dry, extruded, kibble diet twice daily. At each feeding, the following treatments were administered: 1) Control (no FOS or MOS); 2) 1 g FOS; 3) 1 g MOS; or 4) 1 g FOS + 1 g MOS. Fecal, ileal and blood samples were collected during the last 4 d of each 14-d period to measure protein catabolite concentrations, microbial populations, immune characteristics and nutrient digestibilities. Treatment means were compared using preplanned orthogonal contrasts. Dogs supplemented with MOS had lower (P = 0.05) fecal total aerobes and tended to have greater (P = 0.13) Lactobacillus populations. Ileal immunoglobulin (Ig) A concentrations were greater (P = 0.05) in dogs supplemented with FOS + MOS vs. control. Lymphocytes (% of total white blood cells) were greater (P < 0.05) in dogs supplemented with MOS. Serum IgA concentrations also tended (P = 0.13) to be greater in dogs supplemented with MOS. Dogs supplemented with FOS and FOS + MOS had lower (P < 0.05) fecal total indole and phenol concentrations. Dogs supplemented with MOS tended to have lower ileal DM (P = 0.149) and OM (P = 0.146) digestibilities vs. control. Results of this study suggest that dietary supplementation of FOS and MOS may have beneficial effects on colonic health and immune status of dogs.

Animals↗
PubMed1987

An in vivo and in vitro analysis of systemic immune function in mice with histologic evidence of neural transplant rejection.

Histologic and immunocytochemical analyses of fetal neocortical tissue transplanted to the lateral ventricle of inbred adult mice indicate that this tissue survives transplantation well if the donor and host are isogeneic. The major histocompatibility complex (MHC) of the mouse is known as the H-2 locus. H-2-incompatible neural transplants (allografts), unlike their H-2-identical counterpart (isografts), are characterized by the presence of T cells comprising both major T-cell subsets and macrophages, and by a marked increase in the expression of both class I and class II (Ia) MHC antigens. These findings suggest a recognition of H-2 alloantigens by the host's immune system followed by an appropriate effector response. We report here our attempts to demonstrate systemic host sensitization to alloantigens in mice bearing H-2-incompatible intraventricular neural transplants. We measured the time to rejection of orthotopic skin grafts subsequent to neural transplantation, splenocyte proliferative responses to alloantigens in mixed lymphocyte cultures (MLC), and class I-restricted antigen-specific cytolytic T lymphocyte (CTL) activity. No significant differences were found in any of these tests of host systemic sensitization between mice with allogeneic neural transplants and those with isogeneic transplants or control animals. We conclude that intraventricular neural transplants, while recognized and affected by cells of the host's immune system, do not elicit a detectable systemic sensitization to class I H-2 alloantigens. Rejection of neural transplants may depend on sensitization to class II H-2 alloantigens, to so-called minor histocompatibility antigens, or some combination thereof.

Animals↗
PubMed2005

Proteomic analysis of human natural killer cells: insights on new potential NK immune functions.

Applying high-throughput proteomic analysis of mammalian cells can facilitate the identification of a large number of proteins expressed in the examined samples. Moreover, extensive research efforts are being made to perform large-scale characterization of membrane proteins. Here we use mass spectrometry-based proteomic strategy to characterize protein expression in membrane-enriched fractions derived from human NK lymphoma cell line YTS. This query yielded a list of over 1000 identified proteins, and provided us with new insights on NK cell biology. We highlight the expression of CD86 on YTS and its ability to co-stimulate TCR responses of human CD4+ T-cells, providing an unexpected link between innate and adaptive immune systems.

Antigens, CD↗
PubMed2006

Effects of Hydrocotyle sibthorpioides extract on transplanted tumors and immune function in mice.

This paper describes the effects of an ethanolic extract of Hydrocotyle sibthorpioides on transplanted tumors and immunologic function in mice. When the H. sibthorpioides extract was administered orally at a dose of 1.5 or 3.0 g/kg body wt./day for 10 days, the inhibition rates for murine hepatic carcinoma clone (Hep), sarcoma 180 crocker clone (S(180)), and uterine cervical carcinoma clone (U(14)) were significantly enhanced. The antitumor activity of H. sibthorpioides is comparable to that of the common antitumor agent 5-fluorouracil. Also, our results indicate that the H. sibthorpioides extract promoted the thymus and spleen indices, and humoral immunity of mice. These observations demonstrated that H. sibthorpioides exerted a potent inhibitory effect on the growth of tumors, in addition to mediating immunomodulatory effects in mice.

Administration, Oral↗
PubMed1986

Cellular immune function of patients with retinitis pigmentosa.

Although initial investigations of peripheral blood lymphocytes (PBL) from patients with retinitis pigmentosa (RP) demonstrated a reduced percentage of Leu-4 positive (pan-T) lymphocytes, the authors recently determined that the absolute number of Leu-4 positive cells per milliliter of blood is normal. This investigation studied the production of the lymphokines gamma-interferon (gamma-IFN) and interleukin-2 (IL-2) in cultures of concanavalin-A stimulated PBL. The difference in the mean production of gamma-IFN or IL-2 by PBL from 33 RP patients versus PBL from 16 controls did not achieve statistical significance at P less than 0.05. Overall, the data did not demonstrate significant cellular immune abnormalities in patients with RP.

Adolescent↗
PubMed1994

Is immune function better preserved after laparoscopic versus open colon resection?

The purpose of this preliminary study was to evaluate immunologic responses to laparoscopic vs standard open colon resection and to evaluate possible mediators of any differences found. Specifically, we compared cortisol levels and delayed-type hypersensitivity response after each method of colon resection in a group of 20 pigs. Two groups of 10 animals each were treated in identical fashion including bowel preparation, anesthesia, and postoperative management. The only difference between groups was that one underwent laparoscopic and the other an open colon resection. Blood specimens for cortisol were drawn before, during, and immediately postoperatively as well as at 11 A.M. on postoperative days 1 and 2. All animals had been previously immunized as piglets with Sow Bac-E (Oxford Veterinary, Worthington, MN), an antigen preparation of common pig pathogens. At the conclusion of the operative procedure 0.5 cc of the antigen was injected intradermally on the right forelimb of the animals. At 48 and 72 h postoperatively the largest diameters of induration surrounding the injection site were measured and averaged. Cortisol levels were measured in serum samples by radioimmunoassay (Met-Path, Rockville, MD). Statistical significance was determined by t-test. Results of skin antigen testing showed that the group of pigs that underwent laparoscopic resection had a 20% greater response, 1.54 cm +/- 0.28 cm at 48 h and 1.53 cm +/- 0.18 cm at 72 h. For the open-surgery group results were 1.24 cm +/- 0.26 cm at 48 h and 1.32 cm +/- 0.21 cm at 72 h, P < 0.05 for the difference between groups at both 48 and 72 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

T-cell-receptor dose and the time of treatment during murine retrovirus infection for maintenance of immune function.

C57BL/6 mice were injected with different doses of human T-cell receptor (TCR) V beta 8.1 CDR1 peptide at different times after murine retrovirus (LP-BM5) infection. Injection with TCR V beta 8.1 CDR1 peptide largely prevented the retrovirus-induced reduction in B- and T-cell proliferation, and T-helper 1 (Th1) cytokines [interleukin-2 (IL-2) and interferon-gamma (IFN-gamma)] secretion. It also suppressed T-helper 2 (Th2) cytokines (IL-6 and IL-10) production, which was stimulated by retrovirus infection. These effects were accomplished using at least 100 micrograms of peptide per mouse and the most effective dose of peptide had to be given within 4 weeks after retrovirus infection. Immunization with doses above 100 micrograms/mouse as long as 4 weeks postinfection maintained natural killer (NK) cell activity during retrovirus infection. Reducing the dose of peptide or delaying it until the disease progressed towards early murine acquired immune deficiency syndrome (AIDS) allowed development of immune dysfunction. These studies provide data suggesting that immune dysfunction, induced by murine retrovirus infection, was largely prevented by TCR V beta CDR1 peptide injection.

Adjuvants, Immunologic↗
PubMed2002

Mice deficient for the wild-type p53-induced phosphatase gene (Wip1) exhibit defects in reproductive organs, immune function, and cell cycle control.

The Wip1 gene is a serine/threonine phosphatase that is induced in a p53-dependent manner by DNA-damaging agents. We show here that Wip1 message is expressed in moderate levels in all organs, but is present at very high levels in the testes, particularly in the postmeiotic round spermatid compartment of the seminiferous tubules. We have confirmed that Wip1 mRNA is induced by ionizing radiation in mouse tissues in a p53-dependent manner. To further determine the normal biological function of Wip1 in mammalian organisms, we have generated Wip1-deficient mice. Wip1 null mice are viable but show a variety of postnatal abnormalities, including variable male runting, male reproductive organ atrophy, reduced male fertility, and reduced male longevity. Mice lacking Wip1 show increased susceptibility to pathogens and diminished T- and B-cell function. Fibroblasts derived from Wip1 null embryos have decreased proliferation rates and appear to be compromised in entering mitosis. The data are consistent with an important role for Wip1 in spermatogenesis, lymphoid cell function, and cell cycle regulation.

Animals↗
PubMed1989

Transfusion and recipient immune function.

For some time it has been known that allogeneic blood transfusions have immunologic effects on animal and human recipients. These effects include increased numbers of suppressor T cells, decreased natural killer-cell function, decreased function of macrophages and monocytes, induction of anti-idiotypic antibodies that suppress allogeneic antigen recognition, and decreases in alloreactivity of mononuclear cells in mixed lymphocyte cultures. The meaning of these changes is not clearly understood, nor is the exact clinical importance of these alterations known. However, these decreases in immunologic function may explain a number of clinical consequences some investigators believe are the sequelae of homologous blood transfusions. Clinically important outcomes that are associated with transfusions are improved survival of renal allografts and increased risks of bacterial infection and cancer recurrence after perioperative transfusions. Transfusion of plasma-rich blood components (eg, whole blood) has been specifically associated with earlier cancer recurrence and better renal allograft survival in some patient groups. The new hypothesis that transfusion of stored plasma is a major factor in altering host immune defenses is supported by the observation that patients infected with human immunodeficiency acquired immunodeficiency syndrome more rapidly if they have been transfused with large amounts of plasma. Contrary to previous belief, the transfusion of homologous stored blood plasma may have as great or greater effects on immunity than transfusion of white blood cells. We believe investigation into the immunologic effects of transfusions is likely to have a significant impact on transfusion medicine research and practice over the coming years.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Human anti-murine immunoglobulin responses and immune functions in cancer patients receiving murine monoclonal antibody therapy.

In our institution, over 200 patients with gastro-intestinal tract carcinomas have been treated with monoclonal antibodies (MAbs) including CO 17-1A. In one clinical trial, MAbs were administered in combination with gamma interferon. Natural killer cell cytotoxicity (NK) and antibody-dependent cell-mediated cytotoxicity (ADCC) were studied in patients before treatment. Very low NK and ADCC activities were measured in metastatic cancer patients. NK cell lysis was enhanced during gamma-interferon treatment, associated with a modification of the Fc receptor expression, but no changes in the ADCC reactivities of leukocytes were noticed. Monoclonal antibodies were circulating for one to four weeks after a single dose infusion, independent of the patients' immune responses toward the administered MAb. Sixty-three percent of the patients mounted an anti-mouse immunoglobulin response. Anti-idiotypic antibodies were detected in 70% of the responding patients. Variations in the anti-mouse Ig responses were dependent on the therapeutic protocol. The immune responses were composed of IgM, IgA, and IgG (mainly IgG1, often associated with IgG2 and/or IgG3). In patients receiving MAbs together with gamma-interferon, development of the anti-mouse Ig responses were delayed with an increase in the anti-isotypic component and a decrease in the anti-idiotypic component as compared to patients treated with MAb alone. No correlation could be established with clinical results.

Adenocarcinoma↗
PubMed2001

Characterization of CD1d in mucosal immune function: an immunotherapeutic target for inflammatory bowel disease.

In addition to the classical MHC class I and class II molecules, human intestinal epithelial cells also express nonclassical MHC class I-like molecules on their cell surface. CD1d is a non-polymorphic MHC-like molecule whose expression is mainly localized to the epithelial cells of the gastrointestinal tract. The biochemical structure of CD1d on intestinal epithelial cells (IECs) exists in two forms: a 37-kD nonglycosylated, beta 2-microglobulin (beta 2M) independent and a 48-kD glycosylated, beta 2M dependent form. Immunolocalization studies suggest that the 37-kD nonglycosylated form of CD1d is limited to the apical cell surface whereas the 48-50-kD glycosylated, beta 2M dependent form of CD1d is expressed both on the apical and the basolateral surfaces. The beta 2M association with CD1d seems to be important in regulating the pattern of glycosylation and the localization of CD1d within the cell based upon studies of the structure of CD1d in a transfected model cell line and in polarized epithelial cell monolayers. The functional role of intestinal CD1d remains unknown. However, based upon in vitro studies of the antigens presented by human CD1d and mouse CD1d, CD1d expressed on IECs likely presents a very hydrophobic glycolipid molecule possibly from the cell wall of bacteria or host cells. The processed-lipid antigen presented by CD1d may then involve a yet-to-be-identified subpopulation of the resident, oligoclonal alpha beta TCR CD8+ intestinal intraepithelial lymphocyte (iIEL) T cells. Subsequently, these T cells would be very important in regulating the local immune response by producing cytokines and recruiting other immune modulating cells to destroy infected cells, regenerate normal IECs, and possibly downregulate activated T cells to maintain mucosal integrity.

Animals↗
PubMed1989

Comparative effects of roxithromycin and erythromycin on cellular immune functions in vitro. 3. Killing of intracellular Staphylococcus aureus by human macrophages.

The in vitro effect of roxithromycin on the bactericidal activity of human macrophages was compared with that of erythromycin. At a concentration of half the MIC roxithromycin showed a much more impressive killing capacity on macrophage-ingested live Staphylococcus aureus than did erythromycin, under all the experimental conditions used.

Erythromycin↗
PubMed2006

Antitumoral activity of interferon-gamma involved in impaired immune function in cancer patients.

Insufficient immunosurveillance is an important aspect in early tumorigenesis and in the pathogenesis of malignant disease. In the later course of cancer, the development of immunodeficiency is considered the major reason for disease progression and death. Within the anti-tumoral host defense reaction, Th1-type cytokine interferon-gamma (IFN-gamma) is of particular relevance. IFN-gamma stimulates several anti-proliferative and thus tumoricidal biochemical pathways in macrophages and other cells and also in tumor cell lines. These include inducible nitric oxide synthase, indoleamine (2, 3)-dioxygenase, an enzyme degrading the essential amino acid tryptophan, and the production of reactive oxygen species and neopterin in human macrophages and dendritic cells. Although the anti-proliferative strategy of the immune system aims to inhibit the growth of malignant cells, it can also affect T-cell response and thus contribute to the development of immunodeficiency. Accelerated degradation of tryptophan and increased production of neopterin were found to parallel the course of malignant diseases. Moreover, a higher degree of these metabolic changes characterizes poor prognosis and is associated with the development of anemia, weight loss and depressive mood in patients. Available data suggest that immunodeficiency in cancer patients may develop as a long-term side-effect of the antiproliferative and pro-apoptotic mechanisms elicited within Th1-type immune response, and enhanced production of pro-inflammatory cytokine IFN-gamma seems to be critically involved.

Anemia↗
PubMed2005

Prototypic disorders of gastrointestinal mucosal immune function: Celiac disease and Crohn's disease.

Celiac disease is a disorder of the small intestine characterized by chronic inflammation of the mucosa and protean clinical manifestations caused by loss of tolerance to dietary antigens. Two strongly associated cofactors have been identified: the presence of HLA-DQ2 or HLA-DQ8 in the host and specific antigenic peptides in the diet that are present in wheat, rye, and barley. Most patients have complete remission after dietary elimination of these foods. Crohn's disease is characterized by chronic, relapsing, recurrent, focal, transmural inflammation of the gastrointestinal tract that can lead to multiple serious problems requiring chronic medical and surgical therapy. Crohn's disease is associated with multiple genetic mutations, at least one of which has been clearly implicated in innate immunity. Multiple lines of evidence suggest that the disease involves abnormal immune responses to gut microbial flora.

Allergens↗
PubMed1996

Effects of near-infrared radiation on the epidermal proliferation and cutaneous immune function in mice.

While ultraviolet radiation alters various cutaneous cell functions, little is known about the photobiological effects of infrared radiation (IR) on the skin except its local thermal effect. This study demonstrated that single exposure of mouse skin to near IR (0.7-1.3 microns) reversibly suppressed the proliferating activity of the epidermis, the density of Langerhans cells, and the ability of skin to induce contact hypersensitivity reaction. During the exposure, the ear surface temperature was elevated from a mean of 27 to 31.2 degrees C. The results suggest that near IR can modulate the epidermal proliferation and part of the skin immune system, with a mild thermal effect.

Animals↗
PubMed2004

Innate immune functions of the keratinocytes. A review.

Human keratinocytes are known to kill living microbes. They express different pattern recognition receptors (PRRs) such as the Toll-like receptor 2 (TLR2), TLR4, the CD1d molecule and a keratinocyte mannose-binding receptor (KcMR). In response to challenge with microbes or microbial-derived substances the activation and nuclear translocation of NF-kappaB, the production of nitric oxide (NO) and inflammatory cytokines occur in keratinocytes, in a TLR-dependent manner. Blocking of NF-kappaB activation or NO production inhibit the Candida albicans-killing activity of keratinocytes. This Candida killing activity could be inhibited by blocking of KcMR. Recognition of invading pathogens in the epidermis triggers cytokine production in keratinocytes leading to elimination of pathogens and the activation of the adaptive immune system. These findings stress the importance of the role of keratinocytes in innate immunity.

Humans↗