Search PubMed⌕ Search

Biomedical subjects

K Ljunggren

Publications and source records attributed to K Ljunggren.

At least 37 records · Page 2Linked to original sources
PubMed1988

Lack of cross-reaction in antibody-dependent cellular cytotoxicity between human immunodeficiency virus (HIV) and HIV-related West African strains.

Sera from individuals infected with human immunodeficiency virus (HIV) and HIV-related West African viruses can mediate high-titered, virus-specific antibody-dependent cellular cytotoxicity (ADCC) in all stages of infection. No cross-reactive ADCC can be detected between HIV and HIV-related West African strains LAV-2, HTLV-IV, and SBL-6669. Because these two groups of viruses have antigenically distinct envelope glycoproteins, ADCC-mediating antibodies are most likely directed against envelope antigens. For HIV-specific ADCC, this was further confirmed by using sera reacting with HIV envelope but negative for antibodies against viral core antigens.

Africa, Western↗
PubMed1988

Biological significance of the antibody response to HIV antigens expressed on the cell surface.

Human antibodies to HIV antigens expressed on the surface of infected cells may inhibit cell fusion with uninfected CD 4-positive cells and mediate killing of the infected cells by effector cells bearing the Fc receptor. Sequential sera from ten HIV-antibody seroconverted men, of which five progressed to ARC or AIDS (CDC stage IV) during the follow-up period of two years, were tested for the ability to inhibit CD 4-dependent cell fusion, (CFI) and to mediate antibody-dependent cellular cytotoxicity (ADCC). Nine patients developed HIV-specific ADCC and seven CFI-antibodies using the HIV strain HTLV-IIIB as target antigen. These antibodies appeared approximately at the same time 2-12 months after primary infection, defined as antibody seroconversion or antigenaemia. ADCC antibodies were detectable at higher titers as compared to CFI-antibodies. All sera of asymptomatic individuals (CDC stage II and III) were CFI antibody positive and had a higher mean ADCC titer as compared to sera from patients progressing to AIDS or ARC. ADCC and CFI antibodies coincided in some cases in the complete absence of core antibodies. Because the relationship between ADCC and CFI was not exclusive it is concluded that distinct domains of the HIV envelope induce natural antibodies mediating ADCC and CFI.

Acquired Immunodeficiency Syndrome↗
PubMed1988

B and T cell reactivities after immunization of macaques with HIV subcomponents.

A model system was established for studies of humoral and cellular immunity to human immunodeficiency virus (HIV) antigens after vaccination. Macaques (Macaca fascicularis) were immunized with purified HIV, an infected cell extract rich in gp120 or polypeptides of cloned genes representing parts of p24, gp41, and gp120. Western blot analysis best showed the appearance of antibodies to nucleocapsid proteins, and antibodies to higher molecular weight envelope glycoproteins were better demonstrated by radioimmunoprecipitation. With whole HIV, antibodies to p24 appeared first, and sometimes were the only ones to be demonstrable. Several immunizations with HIV or recombinant polypeptides were required to obtain antibodies to gp120, and the responses were weak. Although the envelope-specific response was weak, this was the only component that mediated neutralizing capacity. Escherichia coli-derived viral transmembrane polypeptide (g)p41 also had a poor immunizing effect. IgG synthesis from B cells in vitro was demonstrable to antigens and generally paralleled the antibody titers of sera after multiple immunizations. The HIV-specific lymphocyte proliferation response as measured by DNA synthesis was best seen with polypeptide p24-15, followed by the other antigens.

Animals↗
PubMed1988

Varying antibody response in hospital staff vaccinated against hepatitis B.

Staff from a Department of Infectious Diseases (n = 64) were vaccinated against hepatitis B with HBVax (Merck, Sharp & Dohme), a plasma derived vaccine. Prevaccination testing showed a low prevalence of hepatitis B virus markers (1.4%). Only 1 person showed signs of anamnestic antibody response. Post-exposure prophylaxis and strict hygienic routines are recommended for non-operating hospital staff in areas with low prevalence of hepatitis B virus carriers. The anatomic site of intramuscular administration of the vaccine is discussed. The overall antibody response was low, 83% acquired a protective titer of anti-HBs and only 44% in the age group greater than 40 years of age. Postvaccination testing seems strongly advisable, especially in an older age group.

Adult↗
PubMed1988

Hepatitis delta virus infection in acute hepatitis in Kuwait.

Over a period of 1 year, 254 patients presenting with acute hepatitis at the Infectious Disease Hospital, Kuwait were positive for hepatitis B surface antigen (HBsAg). Of these, 23 (9%) patients were found to have antibodies to hepatitis D virus (HDV) (anti-HDV). Eight of these anti-HDV positive patients were shown to have a coinfection with acute hepatitis B and 8 had a superinfection of HDV on a chronic HBsAg infection. The remaining 7 had had a previous HDV infection and were also chronic carriers of HBsAg. The cause of the acute hepatitis in this group was probably non-A, non-B virus(es). The prevalence of anti-HDV was 4% among patients with acute hepatitis B and 31% among carriers of HBsAg. In the coinfection group, 5/8 patients recovered completely, 1 developed chronic active hepatitis and 1 died due to fulminant hepatitis, while 1 patient was lost to follow up. 5/8 patients with superinfection developed chronic hepatitis on follow-up, 2 died while only 1 patient recovered completely. In the group of patients with previous delta infection, 5/7 recovered from the acute bout of hepatitis while 1 patient developed chronic active hepatitis and 1 was lost to follow-up.

Acute Disease↗
PubMed1988

Neutralizing antibodies in relation to antibody-dependent cellular cytotoxicity-inducing antibodies against human immunodeficiency virus type I.

The presence of neutralizing antibodies against human immunodeficiency virus type 1 (HIV-1) was investigated in sera from 73 HIV-1 seropositive subjects at different clinical stages. Virus neutralization was measured as survival of MT-4 cells in a 6-7 day microassay. Sixty-three sera were also tested for antibodies inducing virus-specific antibody-dependent cellular cytotoxicity (ADCC). Neutralizing antibodies were found in 59% of sera tested, the positivity rate being 50% (9/17) in asymptomatic subjects, 67% (12/18) in patients with persistent generalized lymphadenopathy (PGL) and 54% (14/26) in AIDS patients (not significant differences). ADCC antibodies were present in 43% of the sera. Neutralizing antibodies and ADCC-inducing antibodies were found simultaneously in 35% (22/63) of the sera. Neutralizing antibodies alone were found in 22% (14/63) and ADCC antibodies alone in 6% (4/63) of the sera tested. Thirty-seven per cent (23/63) of the sera were negative for both types of antibodies, 62% of the sera with neutralizing antibodies also had ADCC inducing antibodies and 85% of the sera with ADCC antibodies had neutralizing antibodies. The titres of ADCC antibodies were higher than those of neutralizing antibodies. Thus, the presence of ADCC antibodies was related to the presence of neutralizing antibodies, but no correlation was found between the titres of these antibodies in sera positive for both activities.

AIDS-Related Complex↗
PubMed1988

IgG subclass response to HIV in relation to antibody-dependent cellular cytotoxicity at different clinical stages.

The anti-HIV IgG subclass response was analysed in sera from different clinical stages and related to virus specific antibody-dependent cellular cytotoxicity (ADCC). IgG1 was found to be the dominant subclass, present in all sera and with similar mean titres at different stages. The number of anti-HIV IgG3 positive sera, measured on whole viral lysate antigen plates, decreased during disease progression from 38% in symptom-free to 7% in AIDS patients. IgG2 and IgG4 subclasses were less prevalent although a slight increase of IgG4 frequency was found in AIDS patients. High IgG1 titres correlated with a positive ADCC reaction but there was no correlation between anti-HIV IgG1 and ADCC titres. Some sera which contained HIV IgG1 as the only subclass were able to mediate an ADCC reaction. In addition, when anti-HIV IgG3 was isolated, by protein A chromatography, no ADCC killing was induced by these antibodies. It is concluded that IgG1 is the major ADCC-active IgG subclass in HIV infected individuals. The lack of correlation between IgG1 and ADCC titres may be explained by a relatively small fraction of IgG1 antibodies mediating ADCC.

AIDS-Related Complex↗
PubMed1987

Detection of antibodies which mediate human immunodeficiency virus-specific cellular cytotoxicity (ADCC) in vitro.

A method to detect antibodies which mediate antibody-dependent cellular cytotoxicity (ADCC) against HIV-infected target cells was developed. Normal lymphocytes were used as effector cells and different HIV-infected cell lines as target cells. The level of ADCC varied depending on both the effector cell function and the target cell susceptibility. For evaluation of HIV-specific ADCC, the effector function was simultaneously tested against a standard antigen (beta 2 microglobulin), expressed both on infected and uninfected target cells. The HIV-infected monocytoid cell line U937, clone 2, was found to be the most useful target cell in the present system. The detection of antibodies which induce HIV-specific ADCC killing will permit clinical and experimental analysis of the possible importance of such antibodies in protection against HIV-associated disease symptoms.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Antibody-dependent cellular cytotoxicity-inducing antibodies against human immunodeficiency virus. Presence at different clinical stages.

The presence of antibodies mediating antibody-dependent cellular cytotoxicity (ADCC) against human immunodeficiency virus (HIV)-infected target cells was investigated with 170 sera from patients with varying severity of HIV infection. Approximately 40% of sera from individuals representing all stages of infection were ADCC-positive when tested against HTLV-IIIB infected 0937 clone 2 target cells. The positive sera had higher HIV antibody titers as measured by enzyme-linked immunosorbent assay compared with ADCC-negative sera. ADCC titers were lower in patients with acquired immune deficiency syndrome than in asymptomatic carriers. This decline in ADCC titer was not correlated with a general decrease of HIV antibodies. No correlation between the CD4:CD8 lymphocyte ratio and ADCC activity was found. The possible beneficial effect of ADCC-inducing antibodies early in infection is discussed in relation to the effect of ADCC-inducing antibodies in other retrovirus systems and to the nature of lentivirus infections.

AIDS-Related Complex↗
PubMed1986

Monoclonal antibodies against the NK cell-FcR and the T3-complex potentiate normal lymphocyte killing.

Pretreatment of normal human lymphocytes with monoclonal IgG against the NK cell-FcR (IgG) or the T3 complex was found to potentiate killing of most NK sensitive target cells with the exception of T-cell derived cells. Anti-FcR IgM monoclonals were suppressive for all target cells. IgG anti-FcR mediated potentiation required minute amounts of antibody but was also seen at high anti-FcR concentrations that modulated FcR activity. Potentiated and FcR modulated cells retained anti-FcR IgG on the membrane and conjugated normally to target cells. Anti-FcR potentiation blocked antibody-dependent killing but did not influence lectin-dependent killing, with anti-T3 the opposed effect was seen. Combined anti-FcR and anti-T3 treatment resulted in decreased potentiation. The results suggest that the NK cell-FcR may be activated during normal NK cell killing (without the addition of antibody) as suggested for FcR in B cell triggering.

Antibodies, Monoclonal↗
PubMed1986

Natural killer and T-cell potentiation by monoclonal IgG against natural killer cell FcR(IgG) or the T3 complex.

Treatment of human natural killer (NK) cells with monoclonal antibodies of the IgG isotype against NK cell-FcR(IgG) increased lysis of most haematopoietic target cell lines with high or intermediate background NK susceptibility. Treatment of normal non-adherent lymphocytes with an IgG anti-T3 monoclonal antibody also increased lysis against the same target cells. Potentiating anti-FcR antibodies rapidly modulated FcR activity and the capacity of the cells to act as antibody-dependent killers, although such antibodies were demonstrable for a long time at the cell surface. Anti-FcR treatment did not influence concanavalin A (Con A)-dependent killing, in contrast to anti-T3 treatment, which suppressed lectin-dependent lysis but did not influence antibody-dependent killing. The data is compatible with a 'pro-receptor' theory for FcR in NK killing, stating that such receptors may function in the same way as the T3 complex interacts with specific T cell receptors.

Antibodies, Monoclonal↗
PubMed1984

Single-strain regression analysis for quality control of cephalothin-susceptibility testing and determination of interpretive breakpoints.

Histogram analysis of inhibition zone diameters around the 30 micrograms cephalothin disk for E. coli, P. mirabilis, and K. pneumoniae in samples from 1975 to 1982 showed a marked reproducibility of the disk-diffusion antibiotic-susceptibility test in the routine laboratory. A comparison of interpretive breakpoints with histograms for E. coli, P. mirabilis, K. pneumoniae, S. aureus, coagulase-negative staphylococci, and S. faecalis showed a higher proportion of possible misinterpretations using the breakpoints of the Swedish Reference Group, SRG, as compared to international (NCCLS) breakpoints. Further analysis using single-strain regression analysis revealed two major causes of interpretive errors. Firstly, the laboratory-related regression line for a bacterial species can be different from the general regression line of the reference laboratory. This difference has to be corrected by using species-related breakpoints. For E. coli, a species-specific breakpoint was determined to R = greater than 13 mm. Secondly, MIC limits recommended for the susceptibility categories of cephalothin by SRG are lower than the international limits and close to the true MIC values of many bacterial isolates, leading to misinterpretations due to the methodological variation. These studies suggest an adoption of international MIC limits for the susceptibility categories of cephalothin in Scandinavia. The "I" category should denote an indeterminate zone. A multi-laboratory quality control assessment using histogram analysis is recommended with optional single-strain regression analysis to determine breakpoints for problem combinations of bacterial species and antibiotics.

Bacteria↗
PubMed1980

Liquorrhoea, a review of 66 cases.

Data on liquorrhoea in cases collected in 1947-1977 at the Department of Neurosurgery, University Hospital of Lund, Sweden, are analysed with reference to: 1. Time of onset. 2. Symptoms and signs. 3. Diagnostic methods. 4. Treatment-conservative and surgical. 5. Antibiotic prophylaxis. In more than half of the 66 patients the onset of liquorrhoea was delayed more than one month after the head trauma. Antibiotic prophylaxis to all skull base fractures therefore is questioned. False positive reaction with locally applied test strips is noted. Gammacisternography for localization of the leaking area is recommended. If surgery is performed, a high rate of recurrence can be expected if the supposed leaking area is blindly covered.

Adolescent↗