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Results for “Cellular immune response”

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At least 19 recordsLinked to original sources
PubMed1977

Transfer factor and cellular immune response in urinary tract infections in children.

Cellular immune responses in vivo and in vitro were studied in 20 children with chronic or relapsing urinary tract infections. Skin tests revealed decreased immune responses to PPD in cases with chronic or recurrent pyelonephritis and to OM, in these cases and in cases of lower urinary tract infections. Blast transformation responses to PPD, OM and PHA were at least as high as in controls. Administration of chromatographically purified fraction from human leucocyte transfer factor resulted in a positive skin reaction with antigen concentration, which before TF administration had caused a negative reaction. The results suggest that the action of the transfer factor component used in this study is based on an immunologically nonspecific stimulation of the cellular immune response.

Adolescent↗
PubMed1979

Abnormal cellular immune responses during acquired zinc deficiency.

The cellular immune response of a 17-year-old decerebrate male with acquired zinc deficiency was studied. He had been fed a commercial formula which contained 7.6 mg zinc per kilogram. His caloric intake had been inadequate as judged by his cachexia. A detailed pretreatment nutritional assessment (five separate observations) which included total serum protein and globulins, albumin, folate, vitamins A, B2, C, ceruloplasmin, and plasma zinc, copper, iron, and total iron binding capacity revealed that the patient was deficient only in zinc and calories. His plasma zinc was 41 +/- 5 microgram/d1 compared with our laboratory norm of 89 +/- 9 microgram/d1 for young adult males. Cellular immunity was assessed by delayed skin reactivity to dinitrochlorobenzene and by in vitro lymphocyte transformation studies. Before zinc therapy the patient rendered a negative skin reaction to dinitrochlorobenzene, and the ability of his lymphocytes to undergo blast transformation in response to mitogen stimulation was significantly depressed with a stimulation index of 4.7 +/- 0.8 as compared with 139.1 +/- 77.3 for controls. Within 3 weeks after zinc therapy (22.7 mg zinc per day) he demonstrated a positive delayed skin reaction to dinitrochlorobenzene and a normal lymphocyte response stimulation index = 205.5 +/- 42.6 versus 199.3 +/- 58.2 for control). In addition, a pretreatment facial seborrhea and a decubitus ulcer rapidly healed.

Adolescent↗
PubMed1978

Cellular immune response to cytomegalovirus infection after renal transplantation.

A prospective study of 15 patients who received renal transplants defined the effect of renal transplantation on the cellular immune response to cytomegalovirus infection. Of 15 patients, 14 developed cytomegalovirus infection, usually in the first 2 months after transplantation, and all infections were accompanied by a normal humoral immune response. After the initiation of immunosuppressive therapy and transplantation, there was a general depression of lymphocyte transformation, as reflected in the response to phytohemagglutinin, accompanied by a specific defect in cellular immunity, as indicated by lymphocyte transformation to cytomegalovirus antigen. Eleven patients had cellular immunity to cytomegalovirus before transplantation, and all of these became negative in the first month after transplantation. In subsequent months, only 6 of the 14 study patients with cytomegalovirus infection developed specific cellular immune responses to cytomegalovirus. This occurred most often in patients who had severe febrile illnesses in association with infection. The specific cellular immune response which developed in the posttransplant period did not persist in three of the patients. This study demonstrates the dissociation of the humoral and cellular immune response to cytomegalovirus infection in renal transplant patients and indicates the importance of the loss of cellular immunity in the appearance of infection. Previously infected patients lost their cell-mediated immunity and had reactivation infections despite the presence of serum antibody.

Adult↗
PubMed1979

Cellular immune responses and lymphocyte populations in chronic hepatitis.

Cellular immune responsiveness was examined in chronic persistent hepatitis, chronic active hepatitis and alcoholic liver disease by the use of the lymphocyte transformation test in response to PHA and to allogenic liver mitochondria, inhibition of leukocyte migration, delayed-type skin tests and non-immunospecific granulocyte function tests. Lymphocyte markers, E and EAC rosette forming cells were used for the study of lymphocyte populations. The results have confirmed that the T-cell borne cell-mediated immune function is impaired in chronic active hepatitis, as also in a number of cases of chronic persistent hepatitis.

Adolescent↗
PubMed1976

Discussion paper: specific paralysis of the antitumor cellular immune response produced by growing tumors studied with a radioisotope footpad assay.

The kinetics of the antitumor cellular immune response of mice with progressively growing syngeneic tumors were determined in vivo using a quantitative radioisotopic footpad assay. A close correlation was found between the size of the tumor and the degree of the cellular immune response. An initial phase of cellular immune stimulation was followed by specific suppression and subsequent immunologic paralysis as the tumor grew larger. This immune paralysis was attributed to increased tumor load since a homogenate of an SV40 transformed fibrosarcoma injected intraperitoneally into tumor-immune mice specifically depressed their cellular immune response. The fraction of the tumor homogenate that brought about this depression was present in the high speed supernatant and pellet of a 3M KCl extract of the tumor. The specificity of the depression was determined in vivo by the radioisotopic footpad assay and in vitro by a 51Cr cytolysis assay. Unwashed spleen cells harvested from mice bearing large tumors were unreactive in a local adoptive footpad assay. However, reactivity could be restored by repeatedly washing the spleen cells.

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↗
PubMed1977

Histocompatibility antigens and genetic control of the immune response in guinea-pigs. V. Evidence from further breeding studies for the polygenic control of the cellular immune response to structurally unrelated antigens in the guinea-pig.

Further breeding studies were carried out to investigate the polygenic control of the cellular immune response in the guinea-pig to low doses of aspirin anhydride (ASAN), penicilloylated bovine immunoglobulin (BPO-BGG) and to the multi-chain copolymer (T, G)-A-L. Although responsiveness to these three antigens is controlled by three independently segregating loci, at least one gene required for these responses is linked to the strain 13 haplotype.

Animals↗
PubMed1977

Cellular immune responses in guinea pigs immunized with cell walls of Histoplasma capsulatum prepared by several different procedures.

Since guinea pigs immunized with water-washed cell walls of Histoplasma capsulatum developed cellular immune responses detectable with cytoplasmic substances, attempts were made to determine whether cytoplasmic contamination of the walls was responsible for the induction of the immune response. Cell walls were treated by several procedures designed to remove possible contamination, namely, extraction with lipid solvents, incubation with proteolytic enzymes, and washing with sodium dodecyl sulfate, and each of the treated preparations was compared with water-washed walls for its ability to induce cellular responses demonstrable with cytoplasmic substances. For comparison, wall glycoprotein was also used as a test antigen. Immune responses were assessed by gross and histological examinations of skin test sites and by assays for the production of migration inhibition factor. A portion of the material inducing the response detectable with cytoplasmic substances was apparently removed or altered by each of the purifying procedures. The cellular immune responses to wall glycoprotein were also altered, however, indicating that more than the mere removal of cytoplasmic substances had occurred. On the basis of the data collected from each of the cellular assays involving wall glycoprotein as the test antigen, the hypothesis is proposed that sodium dodecyl sulfate altered or removed protein from the wall and thus augmented its ability to induce a more intense immediate-type hypersensitivity, whereas incubation with Pronase altered the walls in such a way as to shift the balance toward a more intense delayed-type hypersensitivity. The latter effect was probably due to the removal of carbohydrate from the wall by glucanase or to mannosidase contaminating the Pronase preparation.

Animals↗
PubMedDate not supplied

Assessment of cellular immune response to cancer of the breast.

Cellular immune competence and cell-mediated immunity to tumor antigens have been studied in patients with breast cancer. Some patients have been shown to have depressed lymphoproliferative responses to phytohemagglutinin and in mixed leukocyte culture. In some cases, this depression appeared attributable to suppressor cells. Many patients with breast cancer had a cellular immunity to extracts of autologous or allogenetic tumors, as detected by lymphoproliferation and leukocyte migration inhibition assays. In addition, some breast cancer patients reacted to antigens associated with murine mammary tumor virus. Some of the tests for cellular immunity have revealed correlations with clinical course and, therefore, may be of use in the management of patients with breast cancer.

Antigens, Neoplasm↗
PubMed1979

Effects of interferon and adenine arabinoside treatment of hepatitis B virus infection on cellular immune responses.

Fifteen patients with chronic hepatitis B were treated with adenine arabinoside (Ara-A) or human leukocyte interferon (HLI). Cellular immune response to hepatitis B virus surface antigen and antigens prepared from herpes simplex virus, varicella zoster virus, and cytomegalovirus was measured by a lymphocyte blast transformation assay and an assay for interferon production. Measurements were made before, during, and after antiviral treatment. Unlike patients convalescing from acute hepatitis B, only 2 of 15 patients with chronic hepatitis B had significant blast transformation to hepatitis B surface antigen. One such response occurred during the pretreatment period of HLI therapy, and the other was in a patient undergoing low-dose (<10(5) U/kg per day) HLI therapy. Mononuclear cell cultures were tested for interferon production in the presence of hepatitis B surface antigen. Cells from only 1 of 15 patients produced detectable levels of interferon. In contrast, all of these patients had normal cellular immune responses to herpesvirus antigens. Transformation responses to herpes antigens decreased three- to fivefold after patients were treated with >10(5) U of HLI per kg per day. Antiviral therapy with <10(5) U of HLI per kg per day or Ara-A did not produce a detectable depression of transformation response. Ara-A produced marked lymphocytopenia and a marked lymphocyte fragility after 5 or more days of therapy. In vitro Ara-A was toxic to lymphocytes at concentrations as low as 0.5 mug/ml. These changes in lymphocyte parameters may affect the outcome of antiviral therapy.

Acute Disease↗
PubMed1975

Inhibition of the cellular immune response to simian virus 40 tumor cells in tumor-bearing and tumor-immune mice by concanavalin A.

The effects of in vivo-administered concanavalin A (Con A) on the kinetics of the primary and secondary cellular immune responses to simian virus 40-transformed tumor cells were investigated in BALB/c mice. Either a single initial dose of 400 mug Con A or daily doses of 50 mug depressed the cell-mediated immune response to tumor cells during the progressive growth of tumors, as determined by a radioisotopic foot-pad assay. The immune depression correlated with an increase in ultimate tumor weight. Similarly, Con A suppressed the antitumor cellular immune response in tumor-immune animals. Immune reactivity returned within 6 days after a single injection of 400 mug Con. Continuous administration 50 mug Con A resulted in a gradual decline in antitumor cellular immune responsiveness, which reached a plateau by the 5th day. Splenic lymphocytes from Con A-treated, immune mice failed to elicit a local adoptive transfer reaction; their immune responsiveness tended to return after incubation with alpha-methyl-D-pyranosyl sugars.

Animals↗
PubMed1975

Depression of cellular immune response during syngeneic pregnancy as measured by the graft-versus-host reaction.

The cellular immune response during the course of intrastrain pregnancies was evaluated in primiparous and multiparous BALB/c females by the graft-versus-host (GVH) activity of the splenic and lymph nodal lymphocytes. Splenic lymphocytes of both primiparous and multiparous pregnant mice had a GVH activity lower than that of the virgin mice. This immune deficit was more evident in multiparous than in primiparous females and occurred at the 6th day and during the last week of pregnancy. A similar although less pronounced phenomenon was found when lymph nodes instead of spleen of multiparous females were used at the source of cells in GVH reaction. The immune deficit was less marked when spleen and lymph node cells of pregnant mice were compared with similar cells of pseudopregnant females. Incubation of virgin BALB/c spleen lymphocytes in the serum of multiparous pregnant mice as compared to normal virgin serum caused a reduction of the GVH activity; incubation of the cells in pseudopregnant serum also inhibited the immune response, but to a lesser extent than the incubation in multiparous sera.

Animals↗
PubMed1975

Humoral and cellular immune responses to an envelope-associated antigen of herpes simplex virus.

The humoral and cellular immune responses of rabbits and guinea pigs to the envelope-associated antigen of herpes simplex virus type I were studied. Neutralizing antibody (at high titer) and lymphocytes reactive to herpes simplex virus were detected in both guinea pigs and rabbits after immunization with the antigen. In a standard assay of cellular immunity to herpes simplex virus, the antigen stimulated blast transformation of herpes simplex virus-reactive splenic lymphocytes in vitro. Furthermore, immunization of rabbits with the envelope-associated antigen protected the animals from a lethal dose of live herpes simplex virus. Thus an antigen of herpes simplex virus can be prepared which contains neither infectious nor noninfectious viral particles and which stimulates immunity to the virus in laboratory animals.

Animals↗
PubMed1978

Cellular immune response in genital herpes simplex virus infection.

We studied the relations between the cellular immune response, pre-existing complement-fixing antibody and virus type with duration of virus excretion in genital herpes simplex virus (HSV) infection. Thirty-six patients (seven with HSV-1 and 29 with HSV-2) with genital herpes underwent serologic testing, sequential viral cultures and weekly determination of lymphocyte-transformation stimulation index with inactivated HSV antic n. The duration of virus excretion was shortest in those with pre-existing complement-fixing antibody, was unrelated to virus type, and was inversely correlated with the magnitude of the mean peak stimulation index (r = -0.69, P less than 0.001). Prolonged virus excretion occurred in patients with a delayed and diminished peak index. Recurrent episodes had a higher peak index (29.4 compared to 14.5) (P less than 0.02), an earlier development of the peak during recurrences (9.1 vs. 25.8 days) (P less than 0.01) and a briefer duration of viral shedding than initial episodes. Thus, the temporal course and magnitude of the stimulation index correlate with and may determine the duration of genital HSV infection.

Antibodies, Viral↗
PubMed1975

Specific depression of the antitumor cellular immune response with autologous tumor homogenate.

A momogenate of an SV40-transformed firbosarcoma of BALB/c mice (E4 tumor) injected i.p. into E4, tumor-immune syngeneic mice specifically depressed their cell-mediated immune responses to autologous tumor cells, as measured by a radioisotopic foot pad assay. The fraction of the tumor homogenate that brought about this depression was present in the high-speed supernatant and pellet of a 3 M KCl extract of the tumor. The specificity of the depression was shown in three ways: (a) the serum of E4 tumor-immune mice, but not of normal mice, given injections of E4 tumor homogenate 24 hr previously, suppressed antitumor immunity in vitro, as measured by the release of 51Cr from labeled E4 tumor cells incubated with spleen cells from tumor-immune animals; (b) the i.p. inoculation of E4 tumor homogenate did not alter the cellular immune response of tuberculin-sensitized mice to tuberculin; and (c) the i.p. injection of a homogenate of antigenically unrelated tumor did not depress the cellular immune response of E4 tumor-immune mice to E4 tumor cells.

Animals↗
PubMed1979

Studies of the nonspecific cellular immune response in patients with urinary bladder carcinoma. I. PHA-induced lymphocyte transformation.

The nonspecific cellular immune response, as measured by phytohemagglutinin (PHA)-induced blastoid transformation of peripheral lymphocytes in autologous serum, was evaluated in 119 patients with bladder carcinoma and in 21 control subjects. Blastoid transformation was determined by quantifying 3H-thymidine incorporation (counts per minute). The rate of blastogenesis of lymphocytes was shown as the stimulation index which was calculated by dividing the number of counts per minute with PHA by that without PHA. The stimulation index of the control subjects was 29.9 +/- 6.6 (+/- SD); that of the experimental group was 13.3 +/- 7 (significantly lower reactivity). There was a converse correlation between the stimulation index and the grade and stage of tumor. In some cases the change in cellular immunity was compared before and after surgery.

Adult↗