Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:BIOD00082 (IL-2)
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Cytokines that are important in the pathophysiology of allergic diseases are summarized in Table II. The role of certain of these cytokines, especially IL-4 as well as IL-1, IL-2, IL-6, GM-CSF, and TNF-alpha have been documented in nasal biopsies and/or nasal secretions of patients with allergic rhinitis. The improvement of symptoms of allergen rhinitis induced by corticosteroid therapy or immunotherapy were associated with differences in cytokine expression, whereas, steroids decreased IL-4 expression and immunotherapy increased expression of IL-2 and IFN-gamma. These data indicate that these proven therapies most probably are mediated by different mechanisms with different cytokine expression.
Allergy Asthma Proc
PMID:Cytokines and allergic rhinitis. 887 34

There is evidence from epidemiologic studies, supported by more intensive study of selected groups of subjects, for the importance of allergy in initiating and contributing to the severity of bronchial asthma. Furthermore, removal of allergen exposure is followed by improvement in both symptoms and evidence of airway inflammation. Allergen immunotherapy reduces the sensitivity of the respiratory tract to allergens, blocks the influx of eosinophils and mucosal mast cells in response to allergen exposure, and alters the pattern of cytokine release by T-lymphocytes, generally decreasing Th2-related cytokines (IL-4) and increasing those related to the Th1 response (interferon-gamma, IL-2, IL-12). It would be remarkable, given these alterations in responsiveness produced by allergen immunotherapy, if this treatment were not effective in bronchial asthma. Indeed, an analysis of controlled studies of allergen immunotherapy does indicate that it is clinically effective in carefully selected, allergic asthmatics.
Allergy Asthma Proc
PMID:Does allergen immunotherapy have a role in the treatment of bronchial asthma? 919 42

This study investigated cytokine release by T-cell lines from atopic and nonatopic individuals in the presence of specific aeroallergen. Cell lines from atopic and nonatopic individuals secreted IL-2 for less than 14 and more than 21 days, respectively. All of the atopic, but not the nonatopic, cell lines exhibited a biphasic peak in IL-4 and IL-5 secretion. Flow cytometry revealed that, after 35 days, 89.3% of the atopic cells were T helpers and 73.2% were activated. Only 7.4% of the nonatopic cells displayed activation markers. In conclusion, T-cell differentiation may be controlled by other factors in addition to stimulation by aeroallergens.
J Asthma 1998
PMID:The profile of the cytokines secreted during the generation of T-helper cells from atopic asthmatic subjects. 957 45

In recent years there has been an explosive expansion of knowledge relating to a family of proteins involved in the intercellular communication network of the immune system. These substances, referred to as cytokines, are importantly involved in the highly regulated complex sequence of events of cellular interaction that comprise immune responses. Atopic diseases, which afflict 20-30% of the general population, are now considered to be associated with a set of abnormal genetically regulated immune responses to foreign antigens, i.e., allergens. The atopic individuals is characterized by the excessive production of IgE antibody to allergens after inhalation, ingestion, and surface contact. There are now recognized over 19 major classes of cytokines, which have been organized into the following categories according to their major functional activities: 1) Acute phase reactants, promoting and mediating natural immunity (e.g., IL-1, IL-6, TNF, interferons alpha and beta, and IL-8); 2) Cytokines that mediate cellular growth and differentiation (e.g., IL-7, IL-4, IL-2, IL-5, IL-10, IL-12, IL-13); 3) Cytokines that act as hematopoietic growth factors (IL-3, GMCSF, IL-9, IL-11, stem cell factor); 4) Chemokines (alpha and beta major groups, DTG, RANTES); and 5) Cytokines that exert lymphocyte regulatory activity (EG, IFN-gamma, TGF). Of particular importance to allergic disease is the recent recognition of the regulation of helper immune function by two lineages of T helper cells, i.e., Th1 and Th2, by these cytokines. The Th2 hypothesis of allergy (4) considers atopy as a Th2-driven hypersensitivity reaction to allergens of complex genetic and environmental origins, in which the Th1 lineage, normally driven by IL-2, TNF, and IFN-gamma is deficient, and in which a predominant Th2 response is seen that is driven by IL-4, IL-13, IL-5, and IL-10. This knowledge is finding application in both the diagnosis and therapy of allergic diseases, through the measurement or use of cytokines, which may replace deficient quantities, or the use of anticytokines, which may neutralize elevated quantities of cytokines, events that collectively contribute to the immunologic imbalance characteristic of the allergic state. In the future, the application of cytokines will continue to find clinical application in allergic disease, and it behooves the clinical allergist-immunologist to keep abreast of the exciting new developments that are occurring in this field.
Allergy Asthma Proc
PMID:Cytokines and allergic diseases: clinical aspects. 987 71

Intracellular levels of cAMP were found to regulate T cell activity. We examined whether beta2-agonists altered cytokine production and cyclic adenosine monophosphate (cAMP) accumulation in concanavalin A (ConA)-activated peripheral T cells from asthmatic patients. Procaterol and isoproterenol weakly decreased the ConA-elicited interleukin (IL)-4 and IL-5 secretion; however, the inhibitory effect of procaterol on the ConA-induced IL-2 secretion was inferior to that of isoproterenol in normal controls and was little in asthmatics. The intracellular accumulation of cAMP by procaterol was not altered compared with that by isoproterenol. Results suggest that there is a qualitative difference between procaterol- and isoproterenol-induced cAMP accumulation in T cells.
J Asthma 1999 Oct
PMID:Effect of beta-agonists on production of cytokines by activated T cells obtained from asthmatic patients and normal subjects. 1052 46

The neuroendocrine mediators reach the cells of the immune system either through the peripheral circulation or through direct innervation of lymphoid organs. Primary and secondary lymphoid organs are innervated by sympathetic nerve fibers. Lymphocytes and monocytes express receptors for several stress hormones, including CRH, ACTH, cortisol, norepinephrine, and epinephrine. Therefore, it is reasonable to conclude that the neuroendocrine hormones released during a stressful event could alter immune function and subsequently alter the course of immune-based diseases. The impact of psychological stress on immune function has been the subject of extensive research efforts. Using a variety of models from largely healthy humans undergoing various forms of natural and experimental stress models, stress has been associated with suppression of NK activity, mitogen- and antigen-induced lymphocyte proliferation and in vitro production of IL-2 and IFN-gamma. Psychological stress is also associated with a higher rate of in vivo hypoergy to common recall-delayed type hypersensitivity antigens. These studies have suggested that psychological stress suppresses various components of CMI responses. Also, data suggest that chronic stress does not simply suppress the immune system, but induces a shift in the type-1/type-2 cytokine balance toward a predominant type-2 cytokine response. Such a change would favor the inflammatory milieu characteristic of asthma and allergic diseases. Recent studies using well-controlled teenage asthmatic subjects demonstrated immunological changes (decreased NK cell cytotoxicity and cytokine alterations) in response to exam stress. These immune alterations are consistent with a cytokine milieu that could potentially worsen asthma. However, there were no changes in peak flow rates, self-report asthma symptoms, or medication use. The lack of correlation between stress and asthma symptoms may have been related to the timing of the visits in relation to the stressor, the duration of the stressor, disease severity, or a lack of accurate self-report data. Alternatively, stress-mediated exacerbations of asthma may require multiple alterations by stress, including cytokine dysregulation or vagal-mediated airway hyperresponsiveness. The rationale for stress management in asthma is based upon the notion that stress causes a change in immune balance that would favor asthma activity in susceptible individuals. This immune imbalance can be found in TH1/TH2 cytokine changes that occur with stress. Although it has not yet been demonstrated that stress can cause or directly influence the development of asthma, it is interesting to note that both the incidence and prevalence of asthma continue to increase and are higher in urban than in rural areas. Among other differences is the well-appreciated higher chronic stress levels associated with urban living.
Allergy Asthma Proc
PMID:Stress, immune regulation, and immunity: applications for asthma. 1095 92

Interleukin (IL)-16 is a homotetramer of 14-kDa subunits discovered in 1982 as a T-cell-specific chemoattractant factor. IL-16 plays a role in trafficking of several immune cells and may be a major chemotactic signal for CD4+ cells. Here, we review some of the key biological actions of IL-16. Because this cytokine has been shown to affect the levels of many inflammatory mediators such as histamine, serotonin, regulated upon activation, normal T cell expressed and secreted (RANTES), and monocyte chemotactic protein-1 (MCP-1), and other cytokines such as IL-2, we investigated the effect of IL-16 on control and stimulated human umbilical cord blood-derived cultured mast cells after antigen challenge. We found that human recombinant IL-16 (0.2-200 ng/mL) does not affect either basal tryptase or IL-8 release or that induced by anti-immunoglobulin E activation. In accordance with other data in the medical literature, we conclude that the most important function of IL-16 is the chemoattraction of CD4+ cells.
Allergy Asthma Proc
PMID:Interleukin-16 network in inflammation and allergy. 1200 88

Apoptosis regulates inflammatory cell survival in allergic inflammation, and decreased apoptosis contributes to the chronicity of inflammation. To investigate the mechanisms of onset and remission of mite-sensitive childhood asthma, we evaluated peripheral blood mononuclear cell apoptosis in patients with asthma and in remission. There was a similar percentage of hypodiploid cells in unstimulated mononuclear cell cultures from patients with active asthma (29.5+/-5.0%) and normal individuals (25.9+/-4.9%). In contrast, the percentage increased in patients in remission (44.5+/-3.2%). In Dermatophagoides farinae (Df) antigen-stimulated mononuclear cell, the stimulation index was lower in patients with active asthma (0.95+/-0.06%) than in normal individuals (1.31+/-0.16%). In contrast to active patients, the proportion of hypodiploid cells stimulated with Df in patients with remission was equivalent to that of normal controls. After phytohemaglutinin (PHA) stimulation, the percentage of hypodiploid cells in patients with active asthma (35.1+/-3.2%) was also lower than in normal individuals (48.5+/-4.3%) or patients in remission (49.5+/-5.7%). Apoptosis occurred predominantly in CD8+, but not CD4+, cells in patients in remission. Interleukin IL-2 inhibited apoptosis in Df-activated cells in normal individuals, whereas IL-2 did not inhibit apoptosis in cells from patients in remission as well as with active asthma. The expression of Fas receptors on resting mononuclear cells was similar in the three groups. However, Fas receptor expression in Df-stimulated mononuclear cells was greater in patients with active asthma than in healthy individuals. In patients with remission that was equivalent to healthy controls. The PHA increased Fas expression to a similar degree in the three groups. With regard to Fas ligand, the expression was lower in unstimulated cultured mononuclear cells from patients than in normal individuals. In patients in remission that was comparable to normal individuals. The Df stimulation upregulated the Fas ligand in patients with active asthma, and downregulated it in patients in remission. In conclusion, apoptosis in Df-stimulated mononuclear cells is impaired in patients with active asthma, while spontaneous apoptosis of CD8+ cells in vivo is augmented in patients in remission, and may be involved in the onset and remission of mite-sensitive asthma.
J Asthma 2002 Oct
PMID:Induction of peripheral mononuclear cell apoptosis in asthmatic patients in remission. 1244 48

Allergen immunotherapy (IT) results in reduction of symptoms of allergic rhinitis and asthma. There still is not satisfactory evidence as to the best marker that explains clinical responses. IT inhibits the early and late nasal, bronchial, and cutaneous responses to allergen challenge. There are increases in antiallergen immunoglobulin G (IgG; 2- to 10-fold) and IgG4 (10- to 100-fold), a gradual decline in antiallergen IgE antibodies, and reduced numbers of nasal or bronchial mast cells, eosinophils, and CD4+ T-helper 2 (TH2) lymphocytes. Cytokine changes include reductions in serum interleukin (IL)-4 and in vitro lymphocyte-derived IL-4 as compared with a lack of increases in interferon gamma or IL-2. In a study in which skin biopsy specimens were obtained 24 hours after intradermal grass injection, the IT-treated patients had sharply increased numbers of macrophages which had messenger RNA for IL-12. This cytokine supports development of TH0 into TH1 CD4+ lymphocytes. Allergen immunotherapy results in a profound IgG and IgA antibody response with down-regulation of TH2 and possibly up-regulation of TH1 responses.
Allergy Asthma Proc
PMID:Immunotherapy update: mechanisms of action. 1252 1

Aldesleukin is a human recombinant interleukin-2 product. It also is known as interlukin-2 and Proleukin in the United States. It is indicated for the treatment of adults with metastatic renal cell carcinoma as well as for adults with metastatic melanoma. However, its use has been limited because of severe systemic toxicity. There have been no reports of aldesleukin producing a hypersensitivity reaction. This is the first reported case of an immediate systemic hypersensitivity reaction occurring after aldesleukin administration confirmed by enzyme-linked immunosorbent assay for specific immunoglobulin E against aldesleukin.
Allergy Asthma Proc
PMID:Hypersensitivity to aldesleukin (interleukin-2 and proleukin) presenting as facial angioedema and erythema. 1297 98


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