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Biomedical subjects

L Björk

Publications and source records attributed to L Björk.

At least 19 recordsLinked to original sources
PubMed2000

Valerenic acid derivatives and valepotriates among individuals, varieties and species of Valeriana.

To investigate the variations of active compounds between species, varieties and individuals of Valeriana cultivated under the same environmental condition, the contents of valerenic acid derivatives and valepotriates in rhizomes and roots of different plant material were analysed by a HPLC method. Different species or varieties of Valeriana yielded 11.65-0.15 mg/g of valerenic acid derivatives, and 1.81-0.03 mg/g of valepotriates. The variation between individuals of one commercial cultivar of V. officinalis ranged from 12.34 to 3.01 mg/g of valerenic acid derivatives, and 3.67-0.92 mg/g of valepotriates. Individuals from self-pollinated mother plants, normal or regenerated, showed a similar variation. The variation of micropropagated plants was much less than the seed propagated plants. The ratio of mean values between valerenic acid derivatives and valepotriates was similar in all groups (3 < ratio < 8) except one group of micropropagated plants (ratio > 20).

Chromatography, High Pressure Liquid↗
PubMed2000

Changes in antioxidant effects and their relationship to phytonutrients in fruits of sea buckthorn (Hippophae rhamnoides L.) during maturation.

Different fractions of sea buckthorn fruits were investigated for antioxidant activity and its relationship to different phytonutrients. Capacity to scavenge radicals of the crude extract, like the phenolic and ascorbate extracts, decreased significantly with increased maturation. The changes were strongly correlated with the content of total phenolics and ascorbic acid. Antioxidant capacity of the lipophilic extract increased significantly and corresponded to the increase in total carotenoids. The phenolic fractions made a major contribution to the total antioxidant capacity due to the high content of total phenolics. The lipophilic fractions were most effective if the comparison was based on the ratio between antioxidant capacity and content of antioxidants. The crude extract of fruits showed the highest inhibitory effect in both 2,2-azobis(2,4-dimethylvaleronitrile) (AMVN) and ascorbate-iron induced lipid peroxidations. The aqueous and ascorbate-free extracts showed higher inhibition in the AMVN assay, but lower inhibition in ascorbate-iron induced peroxidation, than the lipophilic extract.

Antioxidants↗
PubMed1998

Down-regulation of lymphokine synthesis by intravenous gammaglobulin is dependent upon accessory cells.

We have investigated one mechanism by which pooled human IgG preparations for intravenous use (i.v.Ig) selectively down-regulates lymphokine synthesis. Effects of i.v.Ig on cytokine production were quantified at a cellular level by using an immunocytochemical staining technique. Pure T-lymphocyte preparations (from the peripheral blood of healthy adults) were separated by the use of magnetic beads and were then used in parallel experiments with unfractionated mononuclear cells (MNC). Cell activation was induced either by a combination of the protein kinase C activator, phorbol 12-myristate 13-acetate (PMA), and the calcium ionophore, ionomycin, or by direct ligation of the T-cell receptor, using immobilized anti-CD3 monoclonal antibody (MoAb). Cells were cultured in the presence or absence of i.v.Ig and subsequently harvested and stained for the following cytokines: interleukin-2 (IL-2), interferon-gamma (IFN-gamma), tumour necrosis factor-beta (TNF-beta) and granulocyte-macrophage colony-stimulating factor (GM-CSF). Assessment of the frequencies of positively stained cells was performed by manual microscopy and by computerized image analysis. Activation by PMA/ionomycin or by immobilized anti-CD3 MoAb induced substantial lymphokine production in both MNC and in purified T cells. Addition of i.v.Ig led to a diminished synthesis of all of the T-cell products studied in unfractionated MNC preparations, whereas production was maintained or occasionally increased in the purified T-cell preparations. These findings indicate that the immunomodulatory effect by i.v.Ig on T-cell activation and lymphokine production was dependent on accessory cells.

Adult↗
PubMed1997

Monokine-producing cells predominate in the recruitment phase of NOD insulitis while cells producing Th1-type cytokines characterize the effector phase.

Cells infiltrating the Langerhans' islets of prediabetic NOD females were isolated from 6 weeks to 6 months of age. These cells were assayed at a single-cell level for production of eight different cytokines by intracellular immunofluorescent staining. Quiescent in vivo preactivated cells were detected by in vitro stimulation with PMA and ionomycin for 4 h. The cell recruitment phase, between 6 and 12 weeks of age, is predominated by production of the monokines IL-1alpha, IL-6, and TNF After stimulation IFN-gamma and occasional IL-10 and GM-CSF producing cells could also be observed. This cytokine pattern occurs simultaneously with increasing insulitis, and we suggest that these cytokines are important in attracting inflammatory cells to the islets and maintaining the inflammatory state. A high frequency of endocrine cells producing IL-6 during this period may denote a stress response caused by initial beta-cell destruction due to cytokines released by the inflammatory cells. During the effector phase, between 4 and 6 months, there is a characteristic Th1 cytokine profile with lymphocytes producing IL-2, IFN-gamma and TNF, supposedly TNF-beta. No IL-4 production could be detected and IL-10 was very rarely found, indicating the absence of a Th2 response. Our findings show that the effector phase in NOD insulitis is a Th1 rather than a Th2-mediated event. We also demonstrate that cytokines that may cause initial tissue destruction are produced during the recruitment of inflammatory cells.

Aging↗
PubMed1997

Targeted suppression of cytokine production in monocytes but not in T lymphocytes by a tetravalent guanylhydrazone (CNI-1493).

Image analysis was used to study the cytokine-inhibitory effect of the nitric oxide inhibitor tetravalent guanylhydrazone (CNI-1493) in individual immunocytochemically stained human peripheral blood mononuclear cells (PBMC). CNI-1493 inhibited lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF)-alpha, interleukin (IL)-1alpha, IL-1beta, IL-6, and IL-8 production whether or not LPS stimulation was enhanced by interferon (IFN)-gamma priming. Addition of TNF-alpha to CNI-1493-exposed LPS-stimulated cells partially restored the incidence of IL-1alpha-, IL-1beta-, and IL-8-producing cells. TNF-alpha production induced by costimulation by ligation of CD3 and CD28 was inhibited by CNI-1493 in monocytes but not in T lymphocytes. The prevalence of IL-2-, IFN-gamma-, and TNF-beta-producing T cells was not reduced by CNI-1493. Phorbol ester and ionomycin activation also resulted in a CNI-1493 -induced inhibition of TNF-alpha in monocytes but resistant production of TNF-alpha, IL-2, and IFN-gamma by T cells. Thus, CNI-1493 preferentially inhibited synthesis of proinflammatory cytokines in monocytes.

Cells, Cultured↗
PubMed1996

Fusion of a signal sequence to the interleukin-1 beta gene directs the protein from cytoplasmic accumulation to extracellular release.

Interleukin (IL)-1 differs from most other cytokines by the lack of a signal sequence, which results in the retention of the immature proform intracellularly (i.c.). Several cell types have the capacity to produce IL-1, but release has been shown to be restricted predominantly to monocytes/macrophages and associated with apoptosis of the producer cell. These features have limited the studies on IL-1 in early T cell-APC interactions. To develop a model for studying the biological effects of IL-1 beta release during long-lasting immune responses, we have established cells transfected with IL-1 beta cDNA constructs. To construct a hybrid gene for IL-1 beta release, the signal sequence from the related IL-1 receptor antagonist was fused to the gene encoding the 17-kDa mature form of IL-1 beta. A murine fibroblast cell line was transduced with retroviral technique and analyzed for the expression of human IL-1 beta, with or without a signal sequence (ssIL-1 beta and IL-1 beta, respectively). The fibroblasts transduced with either IL-1 beta or ssIL-1 beta expressed similar levels of human IL-1 beta mRNA. High levels of IL-1 bioactivity were recorded in freeze-thaw extracts from cells expressing the IL-1 beta protein i.c., and in supernatants of ssIL-1 beta-transduced cells, which indicates that the initial formation of a proform of IL-1 beta is not required for correct folding of the protein. Treatment of ssIL-1 beta-transduced cells with Brefeldin A (BFA), an inhibitor of protein transport in the endoplasmatic reticulum, induced accumulation of the protein i.c. BFA treatment did not affect IL-1 beta-transduced cells, while lipopolysaccharide-activated human monocytes increased the secretion of IL-1 beta. Cytoplasmic staining of single cells demonstrated that expression of the ssIL-1 beta gene directed the protein to a perinuclear Golgi-like compartment, whereas cells transduced with IL-1 beta cDNA showed a diffuse cytoplasmic distribution pattern. Secretion of IL-1 beta from human monocytes was under certain conditions accompanied by cell death. In contrast, in the fibroblast cell line transduced to secrete IL-1 beta, no accompanying cell death could be detected. Gene targeting of IL-1 to the secretory or cytoplasmic pathway may be useful for elucidating the role of IL-1 in T cell-APC interactions, avoiding cell death of the producer cells.

3T3 Cells↗
PubMed1996

Synthesis and pharmacology of the enantiomers of UH301: opposing interactions with 5-HT1A receptors.

The (S)-enantiomer of 5-fluoro-8-hydroxy-2-(dipropylamino) tetralin [(S)-2a; (S)-UH301] was the first reported 5-HT1A receptor antagonist. We now give a full account on the synthetic effort leading to the preparation of the racemate and the enantiomers of 2a. The crystal and molecular structure of 2a. HBr has been determined by X-ray diffraction and the absolute configuration has been deduced using statistical tests of the crystallographic R values. The unit cell is tetragonal (P4(1)2(1)2) with a = b = 13.2235(2), c = 39.560(1) A and contains two crystallographically independent molecules in each asymmetric unit. The two solid state conformers differ in the conformation of the N-propyl groups. The pharmacological characterization of the enantiomers was done by use of in vivo biochemical and behavioural assays in rats. The (R)-enantiomer of 2a is a 5-HT1A receptor agonist of low potency while (S)-2a does not exhibit any agonist properties at 5-HT1A receptors. As a consequence of the opposing effects of the enantiomers, the racemate, rac-2a, does not produce any clear-cut effects in rats. The reduced efficacy of (S)-2a as compared to the well known 5-HT1A receptor agonist 8-hydroxy-2-(dipropylamino) tetralin (1;8-OH-DPAT) may be due to the fluoro-substituent induced negative potential of the aromatic ring.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1996

Plasmodium falciparum: differential parasite growth inhibition mediated by antibodies to the antigens Pf332 and Pf155/RESA.

Plasmodium falciparum-reactive antibodies can inhibit growth of parasite blood stages in vitro by interfering at different stages of parasite development. Antibodies reactive with repeat sequences in Pf155/ring-infected surface antigen (Pf155/RESA) or in antigen Pf332 inhibit parasite growth as determined by a reduction of newly infected erythrocytes. Antibodies to Pf155/RESA have been implicated in merozoite invasion inhibition. Since it was considered unlikely that antibodies to the late stage antigen Pf332 act on merozoite invasion, we investigated at what developmental stage this growth inhibition takes place. Parasites were cultured in the presence of antibodies to repeat sequences of either Pf332 or Pf155/RESA and were examined with regard to the distribution of different stages and their morphology. As expected, antibodies to both antigens decreased the number of ring stages after reinfection. They did not affect the intraerythrocytic development of ring stages or trophozoites. However, antibodies to Pf332 induced high levels of schizonts displaying an abnormal morphology while antibodies to Pf155/RESA induced considerably lower levels of degenerated schizonts. Thus, Pf332-reactive antibodies seem to interfere with the schizont development by blocking the rupture of mature schizonts or, alternatively, by interfering intraerythrocytically with late stage parasites.

Amino Acid Sequence↗
PubMed1996

Sendai virus-induced IFN-alpha production analysed by immunocytochemistry and computerized image analysis.

IFN-alpha production in Sendai virus-stimulated human buffy coat cultures could readily be demonstrated in individual cells at a protein level by the use of a novel immuno-enzymatic staining procedure. A distinctive rounded, juxtanuclear staining pattern was generated in producer cells by the accumulation of the intracellularly synthesized IFN-alpha in the Golgi stacks. The technology is based upon acquiring a video image of stained monolayers of cells, viewed in a microscope by a colour camera, which then transfers binary images directly into a computer-controlled operating system. The characteristic appearance of the immunocytochemical staining enabled a computerized image-analysis system to measure IFN-alpha producing cells based on defined criteria set for morphology, intensity, colour and size. The automated system could accurately and reproducibly register a range of 0.1-7.0% of the total cell population as IFN-alpha producing cells during the kinetic studies of the response. Congruent results were obtained with manual microscopy and image analysis concerning the assessment of the incidence of IFN-alpha producing cells in the total cell populations. All IFN-alpha producing cells expressed surface HLA-DR molecules and 95% of these cells belonged to the myelomonocytic lineage. The image analysis system provided, in contrast to conventional microscopy, an opportunity to assess and document differences of signal intensity and cell size of individual IFN-alpha producing as well as non-producing cells.

Cell Size↗
PubMed1996

Metabolic, ventilatory and circulatory effects of doxapram in anaesthetized pigs during normoxia and hypoxia.

BACKGROUND: In a previous clinical study doxapram was found to improve ventilatory efficacy postoperatively, presumably via effects on hypoxic pulmonary vasoconstriction (HPV). The present study was designed to see whether doxapram induced any changes of arterial oxygenation and pulmonary vascular resistance during normoxia or hypoxia and whether the changes were influenced by the anaesthetic agents. METHODS: Seventeen piglets were anaesthetized by combinations of either midazolam + fentanyl + pancuronium + pentobarbital (TIVA, n = 9), or by midazolam + fentanyl + pancuronium + halothane, 0.5% in end-tidal gas (Hal, n = 8). Analyses of expired gas and mixed venous and arterial blood in combination with determinations of central blood flow and pressures allowed for calculations of standard metabolic, ventilatory and circulatory data. Values were obtained at normoventilation using normoxic (FIO2 = 0.3) and hypoxic (FIO2 = 0.08) gas mixtures at calculated doxapram plasma concentrations of 1, 2 and 4 micrograms.ml-1. RESULTS: With few exceptions doxapram administration affected the investigated variables only moderately during normoxia. In group Hal, PVR and SVR showed a biphasic raise (P < 0.05), CO fell (P < 0.05-P > or = 0.05) and C (a-v)O2 rose (P < 0.05). In group TIVA, PaO2 fell (P < 0.01-0.05) despite unchanged PVR, CO and VD/VT. Hypoxia affected a moderate increase in PVR in group TIVA (P < 0.05), which was slightly lower at the lowest and highest plasma levels of doxapram (P < 0.05). In group Hal, the induction of hypoxia induced a more pronounced rise in PVR (P < 0.05) which showed a biphasic response to increasing dose levels of doxapram, the lowest dose affecting a further rise (P < 0.05) and the highest a reduction to values below hypoxia control levels (P < 0.05). Pronounced differences between the two groups with respect to values for metabolic and circulatory variables make the interpretation of data difficult. CONCLUSIONS: Doxapram administration to anaesthetized animals did not induce any effects indicative of augmentation of the HPV response.

Anesthesia↗
PubMed1995

Demonstration of a TH1 cytokine profile in the late phase of NOD insulitis.

Cells infiltrating the Langerhans' islets of prediabetic NOD females were isolated from 6 weeks to 6 months of age. These cells were assayed at a single-cell level for production of eight different cytokines by intracellular immunofluorescent staining. By in vitro stimulation with PMA and ionomycin for 4 hours the method is enhanced also to detect in vivo preactivated cells. During the early phase of insulitis from 6 to 12 weeks of age, mainly the monokines IL-1 alpha, IL-6, and TNF were detected. After stimulation, also IFN-gamma and low numbers of IL-10 and GM-CSF producing cells could be observed, but no IL-2 or IL-4 was seen. This cytokine pattern correlates with an increasing insulitis, and we suggest that these cytokines are important in attracting inflammatory cells to the islets, and may cause initial beta-cell destruction. During a later phase, between 4 and 6 months, there is a characteristic TH1 cytokine profile with production of IL-2 and IFN-gamma occurring after stimulation, as well as lymphocytes producing TNF, supposedly TNF-beta. During this period IL-10 was very rarely observed, and no IL-4 production could be found throughout the study. This indicates the absence of a TH2 cytokine profile in this lesion. In addition IL-6 production occurs in high frequencies at all ages, also in endocrine islet cells. We interpret this as a stress response caused by the inflammatory lesion. Our findings show that the effector phase in NOD insulitis is TH1 rather than TH2 mediated. We also demonstrate that cytokines, that may cause initial tissue destruction, are produced during the recruitment of inflammatory cells.

Aging↗
PubMed1995

Down-regulation of gamma interferon, tumor necrosis factor type I, interleukin 1 (IL-1) type I, IL-3, IL-4, and transforming growth factor beta type I receptors at the local site during the acute phase of Shigella infection.

An immunohistochemical technique was used to examine whether there was a colocalization of cytokine-specific receptors with cytokine-expressing cells. We have previously shown that there is extensive cytokine production and secretion in the rectal mucosa in shigellosis (interleukin 1 alpha [IL-1 alpha], IL-1 beta, IL-1ra, IL-4, IL-6, IL-8, IL-10, tumor necrosis factor alpha [TNF-alpha], TNF-beta, gamma interferon, granulocyte-macrophage colony-stimulating factor, and transforming growth factor beta [TGF-beta]) (R. Raqib, A. A. Lindberg, B. Wretlind, P. K. Bardhan, U. Andersson, and J. Andersson, Infect. Immun. 63:289-296, 1995; R. Raqib, B. Wretlind, J. Andersson, and A. A. Lindberg, J. Infect. Dis. 171:376-384, 1995). Kinetics for receptor expression was compared with that for cytokine synthesis in the inflamed rectal mucosa from Shigella-infected patients during acute (2 to 6 days after onset of diarrhea) and convalescent (30 to 40 days after onset) stages. Quantification of receptor expression was assessed by computer-assisted analysis of video microscopic images. A selective down-regulation of the receptors for gamma interferon, tumor necrosis factor (TNF receptor [TNFR] type I), IL-1 (IL-1 receptor [IL-1R] types I and type II), IL-3, IL-4, and TGF-beta (TGF-beta receptor type I) was observed at the onset of the disease, with a gradual reappearance during the convalescent stage. However, IL-2R, IL-6R, granulocyte-macrophage colony-stimulating factor receptor, TNFR type II, and TGF-beta receptor type II showed no change in expression during the study period and were comparable to controls. Cytokine receptors were predominantly located to the epithelial layer of the mucosal surface and crypts, with variable expression patterns in the lamina propria. A time-dependent kinetic curve was seen for the soluble IL-2R (sIL-2R), sIL-6R, and sTNFR types I and type II shed in stool at the acute stage similar to that observed for cytokine secretion in stool but at four- to six-times-lower concentration. In contrast, soluble receptor levels in plasma were 100-fold higher than the cytokine levels. The results suggest a dissociation in immune regulation between cytokine production and cytokine receptor expression. The down-regulation of the receptors in acute shigellosis was probably a consequence of cytokine-induced internalization and shedding of the receptors during signal transduction as well as due to programmed regulatory roles played by cytokines and the bacterial antigens.

Acute Disease↗
PubMed1994

Quantification of superantigen induced IFN-gamma production by computerised image analysis--inhibition of cytokine production and blast transformation by pooled human IgG.

A quantitative image analysis technique was developed to assess the cytokine content of immunocytochemically stained cytokine producing cells. Peripheral blood mononuclear cells were stimulated to induce cytokine production with the superantigen streptococcal pyrogenic exotoxin-A. We have developed a method based on indirect immunocytochemistry which identifies IFN-gamma producing cells by a characteristic morphology generated by the accumulation of IFN-gamma in the Golgi organelle. An image analysis technique permitted discrimination between these producer cells and IFN-gamma binding target cells, which showed a different appearance, with staining restricted to the cell surface membrane. A semi-automated routine programme allowed the signal from a video camera to be processed by computerised image analysis methodology. This enabled us to measure the number of cytokine producing cells, the cytokine staining intensity in individual cells and the cell size expressed in actual cell area. The incidence of IFN-gamma producing cells determined by image analysis measurement was compared to results obtained using manual microscopy. Cell size was assessed by the image analysis system as well as by flow cytometry. Administration of pooled human IgG for intravenous use (IVIg) to the superantigen stimulated cells significantly down-regulated IFN-gamma production, both in terms of the numbers of producer cells and in terms of cytokine staining intensity in individual cells. In addition blast transformation of cells was substantially reduced. These effects, mediated by IVIg, were also evident following delayed IVIg administration 24 h after the initial cell stimulation.

Adult↗
PubMed1994

Lymphokine production induced by streptococcal pyrogenic exotoxin-A is selectively down-regulated by pooled human IgG.

The influence of pooled human IgG preparations for intravenous use (IVIg) on cytokine production induced by streptococcal pyrogenic exotoxin-A (SPE-A) was studied at the single-cell level using cytokine-specific monoclonal antibodies and indirect immunofluorescence or immunohistochemical staining. Mononuclear cells from healthy adult blood donors were stimulated with SPE-A alone or in the presence of IVIg. IVIg was added either prior to stimulation or 24 h after initiation of cultures, in an attempt to evaluate whether IVIg treatment could influence an already established systemic streptococcal disease. Cells were harvested after 48 or 72 h of culture and stained for the following cytokines: interleukin(IL)-1 alpha, IL-1 beta, IL-1ra, IL-6, IL-8, IL-2, tumor necrosis factor interferon(IFN)-gamma and TNF-alpha and TNF-beta and granulocyte macrophage-colony-stimulating factor. Stimulation with SPE-A lead to extensive lymphokine and monokine production. With the addition of IVIg prior to stimulation there was a strong reduction of blast transformation and an almost complete inhibition of lymphokine production, in particular in the synthesis of IFN-gamma and TNF-beta while the synthesis of IL-1 and IL-8 was either unaffected or increased. Adding IVIg 24 h after SPE-A stimulation also resulted in reduced blast transformation and decreased synthesis of IFN-gamma and TNF-beta. These results indicate an immunomodulatory potential by IVIg on streptococcally induced T cell activation and lymphokine production.

Adult↗
PubMed1994

Does digital chest radiography assess regional ventilation?

Digital radiography of the chest was evaluated for estimation of regional ventilation disturbances. Thirty-three patients with suspected bronchial carcinomas were examined. Objective measurements of regional density changes during breathing correlated significantly with standardized regional lung function tests (133Xe ventilation scintigraphy), but did not permit reliable individual estimations of regional ventilation. About 35% of the density variations could be explained by regional ventilation. Thus, factors other than ventilation, e.g. changes in the geometry of the thorax, have a major impact on the density variation at digital radiography.

Adult↗
PubMed1994

Concomitant in vivo production of 19 different cytokines in human tonsils.

Accumulating data indicate that cytokines, peptides involved in regulation of both physiological and pathological immune responses, are produced predominantly at the site of local antigen stimulation. Cytokine-producing cells were detected at the protein level in human tonsil tissue obtained from children with recurrent tonsillitis or infectious mononucleosis (IM). Concomitant production of 19 different human cytokines, interleukin-1 alpha (IL-1 alpha), IL-1 beta, IL-1 receptor antagonist (ra), IL-2, IL-3, IL-4, IL-5, IL-6, IL-8, IL-10, IL-13, granulocyte-macrophage colony-stimulating factor (GM-CSF), G-CSF, tumour necrosis factor-alpha (TNF-alpha), TNF-beta, interferon-gamma (IFN-gamma) and transforming growth factor-beta 1-3 (TGF-beta 1-3), was identified at a single-cell level by indirect immunohistochemical staining procedures and use of carefully selected cytokine-specific antibodies (Ab). Fresh frozen sections were fixed with 4% paraformaldehyde and permeabilized by 0.1% saponin treatment, eluting cholesterol from the cell-surface membrane and the Golgi complex. The intracellular localization of all cytokines, except IL-1 and IL-1ra, was demonstrated by a characteristic local cytoplasmic perinuclear configuration in producer cells. In addition, the immunoreactivity for certain cytokines (IL-2, IL-4, IL-5, G-CSF and GM-CSF) was expressed on the cell membranes and extended over a large extracellular area encompassing the producer cell. Localization of the cytokine to the Golgi organelle was established by co-staining with a monoclonal antibody (mAb) specific to the Golgi complex. Both the extra- and intracellular cytokine staining reactions could be blocked by preincubation of the cytokine-specific Ab with the corresponding purified natural or recombinant cytokine. A complex cytokine pattern was established in both groups studied, where most T-helper type 1 (Th1) and Th2 lymphokines were expressed in the tonsils but at different frequencies and localizations. Cells expressing IL-4, IL-5, IL-10 and IL-13, (Th2 response) were evident at higher frequencies in recurrent tonsillitis compared to sections from IM, which were associated with a more pronounced IL-2, IFN-gamma and TNF-beta expression.

Acute Disease↗